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Gene Information
Gene symbol: GSTA1
Gene name: glutathione S-transferase alpha 1
HGNC ID: 4626
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1417913 | Effect of insulin and thyroxine on catalase, glutathione-s-transferase, GSH and GSSG in alloxan diabetic rat red cells. |
| 2 | 1417913 | The levels of catalase (CAT), glutathione-s-transferase (GST), reduced glutathione (GSH) and oxidised glutathione (GSSG) were measured in red blood cells from control (C) and diabetic rats (D). |
| 3 | 2523783 | Plasma hepatic glutathione S-transferase concentrations after insulin-induced hypoglycaemia in normal subjects and diabetic patients. |
| 4 | 2523783 | Plasma glutathione S-transferase basic isoenzyme (GST B1) concentrations have been measured by specific radioimmunoassay in Type 1 diabetic patients and in normal subjects, before and after controlled insulin-induced hypoglycaemia, and in a further group of Type 1 diabetic patients in hypoglycaemic coma. |
| 5 | 2523783 | GST B1 concentrations were significantly increased 3 h after controlled insulin-induced hypoglycaemia, both in the diabetic patients (p less than 0.02) and in the normal group (p less than 0.05), but the magnitude of the rise did not differ between these two groups. |
| 6 | 2523783 | Plasma hepatic glutathione S-transferase concentrations after insulin-induced hypoglycaemia in normal subjects and diabetic patients. |
| 7 | 2523783 | Plasma glutathione S-transferase basic isoenzyme (GST B1) concentrations have been measured by specific radioimmunoassay in Type 1 diabetic patients and in normal subjects, before and after controlled insulin-induced hypoglycaemia, and in a further group of Type 1 diabetic patients in hypoglycaemic coma. |
| 8 | 2523783 | GST B1 concentrations were significantly increased 3 h after controlled insulin-induced hypoglycaemia, both in the diabetic patients (p less than 0.02) and in the normal group (p less than 0.05), but the magnitude of the rise did not differ between these two groups. |
| 9 | 7477241 | A significant decrease of malondialdehyde (MDA), reduced (GSH) and oxidized (GSSG) glutathione and reduction of the activities of Se-glutathione peroxidase (Se-GSH-PX, EC. 1.11.1.9.) and glutathione S-transferase (GST, EC. 2.5.1.18.) were observed in kidneys of diabetic rats treated with these vitamins. |
| 10 | 7619052 | To determine whether these mutations might also effect other characteristics of the enzyme, nine MODY-associated mutants were expressed as fusion proteins with Schistosoma japonicum glutathione S-transferase (GST) and compared with three wild-type human GK isoforms that were also expressed in the same manner. |
| 11 | 7710261 | Diabetes resulted in increased cardiac catalase, glutathione S-transferase (GST), copper-zinc superoxide dismutase and manganese superoxide dismutase activities. |
| 12 | 7710261 | Renal catalase levels were decreased in diabetes, while glucose-6-phosphate dehydrogenase activity (G6PDH) was increased. |
| 13 | 7710261 | Diabetes significantly decreased the activities of hepatic GST and G6PDH. |
| 14 | 7710261 | The combination of diabetes and copper deficiency resulted in increased levels of hepatic GST, glutathione peroxidase and glutathione reductase. |
| 15 | 7710261 | Diabetes resulted in increased cardiac catalase, glutathione S-transferase (GST), copper-zinc superoxide dismutase and manganese superoxide dismutase activities. |
| 16 | 7710261 | Renal catalase levels were decreased in diabetes, while glucose-6-phosphate dehydrogenase activity (G6PDH) was increased. |
| 17 | 7710261 | Diabetes significantly decreased the activities of hepatic GST and G6PDH. |
| 18 | 7710261 | The combination of diabetes and copper deficiency resulted in increased levels of hepatic GST, glutathione peroxidase and glutathione reductase. |
| 19 | 7710261 | Diabetes resulted in increased cardiac catalase, glutathione S-transferase (GST), copper-zinc superoxide dismutase and manganese superoxide dismutase activities. |
| 20 | 7710261 | Renal catalase levels were decreased in diabetes, while glucose-6-phosphate dehydrogenase activity (G6PDH) was increased. |
| 21 | 7710261 | Diabetes significantly decreased the activities of hepatic GST and G6PDH. |
| 22 | 7710261 | The combination of diabetes and copper deficiency resulted in increased levels of hepatic GST, glutathione peroxidase and glutathione reductase. |
| 23 | 7726824 | Bovine estrogen receptor binding cyclophilin (ERBC), a cyclophilin component of the unactivated estrogen receptor, has been efficiently expressed in Escherichia coli as a fusion with glutathione S-transferase (GST) and purified by single-step chromatography on glutathione-agarose. |
| 24 | 7726824 | Thrombin cleavage from GST allowed the isolation of purified, recombinant ERBC. |
| 25 | 7726824 | Bovine estrogen receptor binding cyclophilin (ERBC), a cyclophilin component of the unactivated estrogen receptor, has been efficiently expressed in Escherichia coli as a fusion with glutathione S-transferase (GST) and purified by single-step chromatography on glutathione-agarose. |
| 26 | 7726824 | Thrombin cleavage from GST allowed the isolation of purified, recombinant ERBC. |
| 27 | 7961682 | Interactive roles of Ras, insulin receptor substrate-1, and proteins with Src homology-2 domains in insulin signaling in Xenopus oocytes. |
| 28 | 7961682 | Insulin receptor substrate-1 (IRS-1) serves as the major immediate substrate of insulin/insulin-like growth factor (IGF)-1 receptors and following tyrosine phosphorylation binds to specific Src homology-2 (SH2) domain-containing proteins including the p85 subunit of phosphatidylinositol (PI) 3-kinase and GRB2, a molecule believed to link IRS-1 to the Ras pathway. |
| 29 | 7961682 | To investigate how these SH2-containing signaling molecules interact to regulate insulin/IGF-1 action, IRS-1, glutathione S-transferase (GST)-SH2 domain fusion proteins and Ras proteins were microinjected into Xenopus oocytes. |
| 30 | 7961682 | We found that pleiotropic insulin actions are mediated by IRS-1 through two independent, but convergent, pathways involving PI 3-kinase and GRB2. |
| 31 | 7961682 | Thus, microinjection of GST-fusion proteins of either p85 or GRB2 inhibited IRS-1-dependent activation of mitogen-activated protein (MAP) and S6 kinases and oocyte maturation, although only the GST-SH2 of p85 reduced insulin-stimulated PI 3-kinase activation. |
| 32 | 7961682 | Co-injection of a dominant negative Ras (S17N) with IRS-1 inhibited insulin-stimulated MAP and S6 kinase activation. |
| 33 | 7961682 | Micro-injection of activated [Arg12,Thr59]Ras increased basal MAP and S6 kinase activities and sensitized the oocytes to insulin-stimulated maturation without altering insulin-stimulated PI 3-kinase. |
| 34 | 7961682 | These data strongly suggest that IRS-1 can mediate many of insulin's actions on cellular enzyme activation and cell cycle progression requires binding and activation of multiple different SH2-domain proteins. |
| 35 | 7961682 | Interactive roles of Ras, insulin receptor substrate-1, and proteins with Src homology-2 domains in insulin signaling in Xenopus oocytes. |
| 36 | 7961682 | Insulin receptor substrate-1 (IRS-1) serves as the major immediate substrate of insulin/insulin-like growth factor (IGF)-1 receptors and following tyrosine phosphorylation binds to specific Src homology-2 (SH2) domain-containing proteins including the p85 subunit of phosphatidylinositol (PI) 3-kinase and GRB2, a molecule believed to link IRS-1 to the Ras pathway. |
| 37 | 7961682 | To investigate how these SH2-containing signaling molecules interact to regulate insulin/IGF-1 action, IRS-1, glutathione S-transferase (GST)-SH2 domain fusion proteins and Ras proteins were microinjected into Xenopus oocytes. |
| 38 | 7961682 | We found that pleiotropic insulin actions are mediated by IRS-1 through two independent, but convergent, pathways involving PI 3-kinase and GRB2. |
| 39 | 7961682 | Thus, microinjection of GST-fusion proteins of either p85 or GRB2 inhibited IRS-1-dependent activation of mitogen-activated protein (MAP) and S6 kinases and oocyte maturation, although only the GST-SH2 of p85 reduced insulin-stimulated PI 3-kinase activation. |
| 40 | 7961682 | Co-injection of a dominant negative Ras (S17N) with IRS-1 inhibited insulin-stimulated MAP and S6 kinase activation. |
| 41 | 7961682 | Micro-injection of activated [Arg12,Thr59]Ras increased basal MAP and S6 kinase activities and sensitized the oocytes to insulin-stimulated maturation without altering insulin-stimulated PI 3-kinase. |
| 42 | 7961682 | These data strongly suggest that IRS-1 can mediate many of insulin's actions on cellular enzyme activation and cell cycle progression requires binding and activation of multiple different SH2-domain proteins. |
| 43 | 8280723 | Considerably increased levels of malondialdehyde (MDA), as well as of superoxide dismutase (SOD) and catalase (CAT) activity were found in the myocardium of diabetic animals. |
| 44 | 8280723 | The reduced glutathione (GSH) level as well as the activity of glutathione S-transferase (GST) were significantly lower. |
| 45 | 8280723 | CAT and SOD activity values were unchanged. |
| 46 | 8426122 | Glutamic acid decarboxylase (GAD) has been shown to be a target of autoantibodies in insulin-dependent diabetes (IDD). |
| 47 | 8426122 | The central regions of human islet and brain GAD67 (amino acids 208-404) were cloned as fusion proteins with glutathione-S-transferase (GST). |
| 48 | 8826975 | Protein tyrosine phosphatase 1B interacts with the activated insulin receptor. |
| 49 | 8826975 | Protein tyrosine phosphatase 1B (PTP1B) is a protein tyrosine phosphatase of unknown function, although increasing evidence supports a role for this phosphatase in insulin action. |
| 50 | 8826975 | We have investigated the interaction of PTP1B with the insulin receptor using a PTP1B glutathione S-transferase (GST) fusion protein with a point mutation in the enzyme's catalytic domain. |
| 51 | 8826975 | The activated insulin receptor was precipitated from purified receptor preparations and whole-cell lysates by the inactive PTP1B-GST, demonstrating a direct association between the insulin receptor and PTP1B. |
| 52 | 8826975 | A p120 of unknown identity was also precipitated from whole-cell lysates by the PTP1B fusion protein, but IRS-1 (pp185) was not. |
| 53 | 8826975 | A catalytically inactive [35S]PTP1B-fusion protein bound directly to immobilized insulin receptor kinase domains and was displaced in a concentration-dependent manner. |
| 54 | 8826975 | Finally, tyrosine-phosphorylated PTP1B was precipitated from whole-cell lysates by an anti-insulin receptor antibody after insulin stimulation. |
| 55 | 8826975 | The site of interaction between PTP1B and the insulin receptor was studied using phosphopeptides modeled after the receptor's kinase domain, the NPXY domain, and the COOH-terminal. |
| 56 | 8826975 | Study of mutant insulin receptors demonstrated that activation of the kinase domain is necessary for the PTP1B:insulin receptor interaction, but receptors with deletion of the NPXY domain or of the COOH-terminal can still bind to the PTP1B-GST. |
| 57 | 8826975 | We conclude that PTP1B can associate directly with the activated insulin receptor at multiple different phosphotyrosine sites and that dephosphorylation by PTP1B may play a significant role in insulin receptor signal transduction. |
| 58 | 8937480 | Effect of bitter melon (Momordica charantia) fruit juice on the hepatic cytochrome P450-dependent monooxygenases and glutathione S-transferases in streptozotocin-induced diabetic rats. |
| 59 | 8937480 | In the present study, we have investigated the effects of oral feeding of karela fruit juice on the hepatic cytochrome P450 (CYP) and glutathione S-transferase (GST) drug-metabolizing enzymes in the streptozotocin (STZ)-induced diabetic rat. |
| 60 | 8937480 | Western immunoblot analysis of CYP and GST isozymes exhibited a differential response during diabetes. |
| 61 | 8937480 | The expression of CYP1A1, 2B1, 2E1, 3A4, and 4A2 in diabetes, while a decrease in GST mu was observed. |
| 62 | 8937480 | Our results suggest that the changes in hepatic phase I and phase II drug-metabolizing enzyme activities in the STZ-induced diabetic animals may be associated with the altered expression of different CYP and GST isozymes. |
| 63 | 8937480 | Effect of bitter melon (Momordica charantia) fruit juice on the hepatic cytochrome P450-dependent monooxygenases and glutathione S-transferases in streptozotocin-induced diabetic rats. |
| 64 | 8937480 | In the present study, we have investigated the effects of oral feeding of karela fruit juice on the hepatic cytochrome P450 (CYP) and glutathione S-transferase (GST) drug-metabolizing enzymes in the streptozotocin (STZ)-induced diabetic rat. |
| 65 | 8937480 | Western immunoblot analysis of CYP and GST isozymes exhibited a differential response during diabetes. |
| 66 | 8937480 | The expression of CYP1A1, 2B1, 2E1, 3A4, and 4A2 in diabetes, while a decrease in GST mu was observed. |
| 67 | 8937480 | Our results suggest that the changes in hepatic phase I and phase II drug-metabolizing enzyme activities in the STZ-induced diabetic animals may be associated with the altered expression of different CYP and GST isozymes. |
| 68 | 8937480 | Effect of bitter melon (Momordica charantia) fruit juice on the hepatic cytochrome P450-dependent monooxygenases and glutathione S-transferases in streptozotocin-induced diabetic rats. |
| 69 | 8937480 | In the present study, we have investigated the effects of oral feeding of karela fruit juice on the hepatic cytochrome P450 (CYP) and glutathione S-transferase (GST) drug-metabolizing enzymes in the streptozotocin (STZ)-induced diabetic rat. |
| 70 | 8937480 | Western immunoblot analysis of CYP and GST isozymes exhibited a differential response during diabetes. |
| 71 | 8937480 | The expression of CYP1A1, 2B1, 2E1, 3A4, and 4A2 in diabetes, while a decrease in GST mu was observed. |
| 72 | 8937480 | Our results suggest that the changes in hepatic phase I and phase II drug-metabolizing enzyme activities in the STZ-induced diabetic animals may be associated with the altered expression of different CYP and GST isozymes. |
| 73 | 8937480 | Effect of bitter melon (Momordica charantia) fruit juice on the hepatic cytochrome P450-dependent monooxygenases and glutathione S-transferases in streptozotocin-induced diabetic rats. |
| 74 | 8937480 | In the present study, we have investigated the effects of oral feeding of karela fruit juice on the hepatic cytochrome P450 (CYP) and glutathione S-transferase (GST) drug-metabolizing enzymes in the streptozotocin (STZ)-induced diabetic rat. |
| 75 | 8937480 | Western immunoblot analysis of CYP and GST isozymes exhibited a differential response during diabetes. |
| 76 | 8937480 | The expression of CYP1A1, 2B1, 2E1, 3A4, and 4A2 in diabetes, while a decrease in GST mu was observed. |
| 77 | 8937480 | Our results suggest that the changes in hepatic phase I and phase II drug-metabolizing enzyme activities in the STZ-induced diabetic animals may be associated with the altered expression of different CYP and GST isozymes. |
| 78 | 8960251 | The activity of cytosol glutathione S-transferase (GST) was decreased to 55% of the control with p-nitrobenzyl chloride, and was unchanged with 1-chloro-2,4-dinitrobenzene, and ethacrynic acid. |
| 79 | 8960251 | The activity of GST and cytosol Se-GSHPx, as well as GSH content, returned to a normal values after insulin treatment, while the activity of non Se-GSHPx was reduced of about 50% in relation to the control values. |
| 80 | 8960251 | The activity of cytosol glutathione S-transferase (GST) was decreased to 55% of the control with p-nitrobenzyl chloride, and was unchanged with 1-chloro-2,4-dinitrobenzene, and ethacrynic acid. |
| 81 | 8960251 | The activity of GST and cytosol Se-GSHPx, as well as GSH content, returned to a normal values after insulin treatment, while the activity of non Se-GSHPx was reduced of about 50% in relation to the control values. |
| 82 | 8960250 | Cytosolic liver glutathione S-transferase (GST) activity was decreased for CDNB and DCNB as substrates in long term alloxan induced diabetes. |
| 83 | 8960250 | After insulin treatment of diabetic animals the activities of both cytosolic and microsomal GST was not restored and the activity of non Se-GSHPx was significantly lower than the control value. |
| 84 | 8960250 | Cytosolic liver glutathione S-transferase (GST) activity was decreased for CDNB and DCNB as substrates in long term alloxan induced diabetes. |
| 85 | 8960250 | After insulin treatment of diabetic animals the activities of both cytosolic and microsomal GST was not restored and the activity of non Se-GSHPx was significantly lower than the control value. |
| 86 | 9185878 | High T cell responses to the glutamic acid decarboxylase (GAD) isoform 67 reflect a hyperimmune state that precedes the onset of insulin-dependent diabetes. |
| 87 | 9185878 | Pancreatic islet beta-cell destruction leading to insulin-dependent diabetes mellitus (IDDM) is an autoimmune T cell-mediated process. |
| 88 | 9185878 | Peripheral blood T cells, which proliferate to islet antigens such as glutamic acid decarboxylase (GAD), (pro)insulin or tyrosine phosphatase IA-2, can be detected in at-risk, first degree relatives of people with IDDM. |
| 89 | 9185878 | Peripheral blood T cell responses to a GAD67(aa208-404)-glutathione-S-transferase (GST) fusion protein, GST, insulin and tetanus toxoid were measured, together with antibodies to islet cells, GAD, insulin and IA-2. |
| 90 | 9185878 | High levels of antibodies to GAD or insulin were generally associated with low T cell responses to these antigens. |
| 91 | 9185878 | Relatives who developed IDDM were characterized by high levels of antibodies to insulin and/or islet cells, and high T cell responses to GAD67-GST and tetanus, but not insulin, in the 24 months before clinical diagnosis. |
| 92 | 9350055 | This diabetes-induced change was associated with a marked impairment in the hepatic glutathione antioxidant/detoxification response to CCl4 challenge, as indicated by the abrogation of the increases in hepatic reduced glutathione (GSH) level, glucose-6-phosphate dehydrogenase and microsomal glutathione S-transferases (GST) activities upon challenge with increasing doses of CCl4. |
| 93 | 9367667 | Catalase (CAT) activity was not significantly affected in any of the tissues in diabetic and insulin-treated animals, however, CAT activity markedly increased in tissues with C. decidua treatment. |
| 94 | 9367667 | However, glutathione (GSH) content in the heart and kidney and glutathione reductase (GSH-R) activity in all the tissues studied increased in diabetic rats while treatment with insulin lowered GSH content and GSH-R activity in these tissues. |
| 95 | 9367667 | Glutathione S-transferase (GST) was not significantly affected in diabetic rat tissue, however, heart GST increased with antidiabetic treatments. |
| 96 | 9367667 | The increase in glucose-6-phosphate dehydrogenase (G6PDH) in the kidney and heart of diabetic rats subsequently decreased with C. decidua treatment. |
| 97 | 9467831 | Cytochrome P450-dependent oxidation and glutathione conjugation of xenobiotics in alloxan-induced diabetic rat. |
| 98 | 9467831 | The status of cytochrome P450-dependent oxidative biotransformation of aminopyrine and benzo(a)pyrene (Phase I reaction) and glutathione S-transferase (GST) catalyzed conjugation with 1-chloro-2,4-dinitrobenzene (CDNB) (Phase II reaction) was evaluated in diabetic rats sacrificed 3 weeks after alloxan treatment (2 doses of 75 mg/kg at an interval of 48 h, i.p.). |
| 99 | 9480911 | Interaction in vitro of the product of the c-Crk-II proto-oncogene with the insulin-like growth factor I receptor. |
| 100 | 9480911 | The Crk proto-oncogene product is an SH2 and SH3 domain-containing adaptor protein. |
| 101 | 9480911 | We have previously demonstrated that Crk-II becomes rapidly tyrosine-phosphorylated in response to stimulation with insulin-like growth factor I (IGF-I) and might be involved in the IGF-I receptor signalling pathway. |
| 102 | 9480911 | To determine whether this involvement includes the direct interaction of Crk-II with the cytoplasmic region of the receptor, studies were performed in vitro with glutathione S-transferase (GST) fusion proteins containing various domains of Crk-II. |
| 103 | 9480911 | The kinase assay in vitro showed that activated IGF-I receptors efficiently phosphorylated the GST-Crk-II fusion protein. |
| 104 | 9480911 | Different domains of the IGF-I receptor were expressed as (His)6-tagged fusion peptides, phosphorylated with activated wheat germ agglutinin-purified IGF-I receptors and tested for association with GST-Crk-II fusion proteins. |
| 105 | 9480911 | Interaction in vitro of the product of the c-Crk-II proto-oncogene with the insulin-like growth factor I receptor. |
| 106 | 9480911 | The Crk proto-oncogene product is an SH2 and SH3 domain-containing adaptor protein. |
| 107 | 9480911 | We have previously demonstrated that Crk-II becomes rapidly tyrosine-phosphorylated in response to stimulation with insulin-like growth factor I (IGF-I) and might be involved in the IGF-I receptor signalling pathway. |
| 108 | 9480911 | To determine whether this involvement includes the direct interaction of Crk-II with the cytoplasmic region of the receptor, studies were performed in vitro with glutathione S-transferase (GST) fusion proteins containing various domains of Crk-II. |
| 109 | 9480911 | The kinase assay in vitro showed that activated IGF-I receptors efficiently phosphorylated the GST-Crk-II fusion protein. |
| 110 | 9480911 | Different domains of the IGF-I receptor were expressed as (His)6-tagged fusion peptides, phosphorylated with activated wheat germ agglutinin-purified IGF-I receptors and tested for association with GST-Crk-II fusion proteins. |
| 111 | 9480911 | Interaction in vitro of the product of the c-Crk-II proto-oncogene with the insulin-like growth factor I receptor. |
| 112 | 9480911 | The Crk proto-oncogene product is an SH2 and SH3 domain-containing adaptor protein. |
| 113 | 9480911 | We have previously demonstrated that Crk-II becomes rapidly tyrosine-phosphorylated in response to stimulation with insulin-like growth factor I (IGF-I) and might be involved in the IGF-I receptor signalling pathway. |
| 114 | 9480911 | To determine whether this involvement includes the direct interaction of Crk-II with the cytoplasmic region of the receptor, studies were performed in vitro with glutathione S-transferase (GST) fusion proteins containing various domains of Crk-II. |
| 115 | 9480911 | The kinase assay in vitro showed that activated IGF-I receptors efficiently phosphorylated the GST-Crk-II fusion protein. |
| 116 | 9480911 | Different domains of the IGF-I receptor were expressed as (His)6-tagged fusion peptides, phosphorylated with activated wheat germ agglutinin-purified IGF-I receptors and tested for association with GST-Crk-II fusion proteins. |
| 117 | 9513449 | [Glutathione S-transferase (GST)]. |
| 118 | 9531526 | Effects of gestational and overt diabetes on human placental cytochromes P450 and glutathione S-transferase. |
| 119 | 9531526 | Animal and in vivo studies have observed that the presence of diabetes alters the expression of hepatic metabolizing enzymes (cytochrome P450 and glutathione S-transferase); however, it is unknown whether similar alterations occur in the human placenta. |
| 120 | 9531526 | To evaluate whether diabetes has any effect of placental xenobiotic metabolizing activity, the catalytic activities of 7-ethoxyresorufin O-deethylation (EROD, CYP1A1), chlorzoxazone 6-hydroxylation (CYP2E1), dextromethorphan N-demethylation (CYP3A4), dextromethorphan O-demethylation (CYP2D6), and 1-chloro-2, 4-dinitrobenzene (CDNB) conjugation with glutathione (glutathione S-transferase, GST) from placentas of diet (class A1) and insulin-dependent (class A2) gestational diabetics and overt diabetics were compared with matched controls. |
| 121 | 9531526 | In contrast to that observed with CYP1A1, a small but statistically significant reduction in GST activity was noted in overt diabetics as compared with their matched controls and gestational diabetics. |
| 122 | 9531526 | GST protein was detectable in all tissues studied, but no CYP protein could be detected in any of the tissues. |
| 123 | 9531526 | Effects of gestational and overt diabetes on human placental cytochromes P450 and glutathione S-transferase. |
| 124 | 9531526 | Animal and in vivo studies have observed that the presence of diabetes alters the expression of hepatic metabolizing enzymes (cytochrome P450 and glutathione S-transferase); however, it is unknown whether similar alterations occur in the human placenta. |
| 125 | 9531526 | To evaluate whether diabetes has any effect of placental xenobiotic metabolizing activity, the catalytic activities of 7-ethoxyresorufin O-deethylation (EROD, CYP1A1), chlorzoxazone 6-hydroxylation (CYP2E1), dextromethorphan N-demethylation (CYP3A4), dextromethorphan O-demethylation (CYP2D6), and 1-chloro-2, 4-dinitrobenzene (CDNB) conjugation with glutathione (glutathione S-transferase, GST) from placentas of diet (class A1) and insulin-dependent (class A2) gestational diabetics and overt diabetics were compared with matched controls. |
| 126 | 9531526 | In contrast to that observed with CYP1A1, a small but statistically significant reduction in GST activity was noted in overt diabetics as compared with their matched controls and gestational diabetics. |
| 127 | 9531526 | GST protein was detectable in all tissues studied, but no CYP protein could be detected in any of the tissues. |
| 128 | 9531526 | Effects of gestational and overt diabetes on human placental cytochromes P450 and glutathione S-transferase. |
| 129 | 9531526 | Animal and in vivo studies have observed that the presence of diabetes alters the expression of hepatic metabolizing enzymes (cytochrome P450 and glutathione S-transferase); however, it is unknown whether similar alterations occur in the human placenta. |
| 130 | 9531526 | To evaluate whether diabetes has any effect of placental xenobiotic metabolizing activity, the catalytic activities of 7-ethoxyresorufin O-deethylation (EROD, CYP1A1), chlorzoxazone 6-hydroxylation (CYP2E1), dextromethorphan N-demethylation (CYP3A4), dextromethorphan O-demethylation (CYP2D6), and 1-chloro-2, 4-dinitrobenzene (CDNB) conjugation with glutathione (glutathione S-transferase, GST) from placentas of diet (class A1) and insulin-dependent (class A2) gestational diabetics and overt diabetics were compared with matched controls. |
| 131 | 9531526 | In contrast to that observed with CYP1A1, a small but statistically significant reduction in GST activity was noted in overt diabetics as compared with their matched controls and gestational diabetics. |
| 132 | 9531526 | GST protein was detectable in all tissues studied, but no CYP protein could be detected in any of the tissues. |
| 133 | 9755800 | Levels of blood glucose, lipid peroxidation, glutathione (GSH), glutathione peroxidase (GPx), glutathione S-transferase (GST) activities and blood selenium levels were determined in streptozotocin (STZ)-induced diabetic mice. |
| 134 | 9819130 | Glutathione S-transferase (GST) is commonly used as a fusion partner in producing recombinant proteins and this technology is increasingly being used to produce antigens for use in immunoassays to measure antibodies. |
| 135 | 9891847 | Hexokinase, glucose-6-phosphate dehydrogenase and antioxidant enzymes in diabetic reticulocytes: effects of insulin and vanadate. |
| 136 | 9891847 | The activities of hexokinase (HK) and glucose-6-phosphate dehydrogenase (G-6PDH) were increased in reticulocyte hemolysate isolated from the diabetic rats and were restored to normal levels by insulin. |
| 137 | 9891847 | The enzymes of glutathione metabolism namely glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-s-transferase (GST) exhibited increases in their activities with diabetes and were restored to almost control values by insulin treatment. |
| 138 | 9891847 | The level of superoxide dismutase(SOD) decreased in the reticulocytes of diabetic rats and catalase (CAT) was unchanged. |
| 139 | 9891847 | Both CAT and SOD had normal values when the diabetic rats were treated with insulin and vanadate. |
| 140 | 9915838 | Using an in situ electroporation system which permits the introduction of glutathione S-transferase (GST) fusion proteins into cells, we found that c-CrkII bound to p130(cas), but not to paxillin in serum-starved rat-1 fibroblasts overexpressing the human insulin receptor (HIRc cells) in vivo. 17 nM insulin stimulation dissociated the binding of c-CrkII to p130(cas), whereas 13 nM insulin-like growth factor-I, 16 nM epidermal growth factor (EGF), and 10% serum each showed little or no effect. |
| 141 | 9915838 | Microinjection of either GST-Crk-SH2 or -Crk-(N)SH3 domains, or anti-Crk antibody each inhibited stress fiber formation before and after insulin-like growth factor-I, EGF, and serum stimulation. |
| 142 | 9915838 | Microinjection of the Crk-inhibitory reagents also inhibited DNA synthesis after insulin-like growth factor-I, EGF, and serum stimulation, but not after insulin. |
| 143 | 9915838 | Using an in situ electroporation system which permits the introduction of glutathione S-transferase (GST) fusion proteins into cells, we found that c-CrkII bound to p130(cas), but not to paxillin in serum-starved rat-1 fibroblasts overexpressing the human insulin receptor (HIRc cells) in vivo. 17 nM insulin stimulation dissociated the binding of c-CrkII to p130(cas), whereas 13 nM insulin-like growth factor-I, 16 nM epidermal growth factor (EGF), and 10% serum each showed little or no effect. |
| 144 | 9915838 | Microinjection of either GST-Crk-SH2 or -Crk-(N)SH3 domains, or anti-Crk antibody each inhibited stress fiber formation before and after insulin-like growth factor-I, EGF, and serum stimulation. |
| 145 | 9915838 | Microinjection of the Crk-inhibitory reagents also inhibited DNA synthesis after insulin-like growth factor-I, EGF, and serum stimulation, but not after insulin. |
| 146 | 10230044 | In liver, Glutathione Peroxidase and Superoxide Dismutase decreased and in intestine Glutathione-S-transferase (GST) increased by diabetes. |
| 147 | 10343979 | The content of glutathione (GSH) and its synthesizing enzyme gamma-glutamylcystein synthetase and also superoxide dismutase (SOD) and catalase activities (reactive oxygen scavenging enzymes) were significantly decreased from almost all the brain regions studied. |
| 148 | 10343979 | However, glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), gamma-glutamyl transpeptidase (gamma-GTP), and glutamine synthetase (GS) activities were increased in the diabetic rat brain. |
| 149 | 10711628 | We studied the long-term effects of streptozotocin-induced diabetes on tissue-specific cytochrome P450 (CYP) and glutathione-dependent (GSH-dependent) xenobiotic metabolism in rats. |
| 150 | 10711628 | During diabetes an increased expression of CYP1A1, CYP2E1, and CYP4A1 isoenzymes was also seen by Western blot analysis. |
| 151 | 10711628 | A marked decrease (65%) in hepatic GSH content and glutathione S-transferase (GST) activity and an increase (about two-fold) in brain GSH and GST activity was observed in diabetic rats. |
| 152 | 10711628 | Karela-juice feeding, in general, reversed the effect of chronic diabetes on the modulation of both P450-dependent monooxygenase activities and GSH-dependent oxidative stress related LPO and GST activities. |
| 153 | 10711628 | We studied the long-term effects of streptozotocin-induced diabetes on tissue-specific cytochrome P450 (CYP) and glutathione-dependent (GSH-dependent) xenobiotic metabolism in rats. |
| 154 | 10711628 | During diabetes an increased expression of CYP1A1, CYP2E1, and CYP4A1 isoenzymes was also seen by Western blot analysis. |
| 155 | 10711628 | A marked decrease (65%) in hepatic GSH content and glutathione S-transferase (GST) activity and an increase (about two-fold) in brain GSH and GST activity was observed in diabetic rats. |
| 156 | 10711628 | Karela-juice feeding, in general, reversed the effect of chronic diabetes on the modulation of both P450-dependent monooxygenase activities and GSH-dependent oxidative stress related LPO and GST activities. |
| 157 | 10804329 | SO(2) exposure, while markedly decreasing Cu, Zn-Superoxide dismutase (Cu, Zn-SOD) activity, significantly increased glutathione peroxidase (GSH-Px), catalase (CAT), glutathione (GSH) and glutathione-s-transferase (GST) activities and TBARS values in CSO(2) and DSO(2) groups compared with their respective control groups. |
| 158 | 10812837 | Polymorphism and the induction/inhibition of drug-metabolizing enzymes, such as cytochrome P450, aldehyde dehydrogenase (ALDH), glutathione S-transferase (GST), N-acetyltransferase (NAT), and NAD(P)H-quinone oxidoreductase (NQO1), were reviewed in relation to susceptibility to disease and to inter-individual difference in biological monitorings. |
| 159 | 10812837 | Investigation of such situations has generated data implicating GSTT1, GSTM1, NAT2, and NQO1 polymorphisms in biological monitoring of some chemicals; the ALDH2 polymorphism is the likely link between the genotype and the metabolism of low molecular aliphatic aldehydes. |
| 160 | 10838356 | Effects of gestational and overt diabetes on placental cytochromes P450 and glutathione S-transferase. |
| 161 | 10838356 | Objective: Animal and in vivo human studies have observed that diabetes alters the expression of hepatic metabolizing cytochrome P450 (CYP) and glutathione S-transferase (GST) enzymes. |
| 162 | 10838356 | Our objective was to compare placental xenobiotic metabolizing activity in diabetics to matched non-diabetic controls to determine if the presence of diabetes alters placental xenobiotic metabolizing activity.Methods: The catalytic activities of 7-ethoxyresorufin-O-deethylation [EROD] (CYP1A1), chlorzoxazone 6-hydroxylation (CYP2E1), dextromethorphan N-demethylation (CYP3A4), dextromethorphan O-demethylation (CYP2D6), and 1-chloro-2,4-dinitrobenzene (CDNB) conjugation with glutathione (GST) from placentas of diet controlled (class A1) and insulin-dependent (class A2) gestational diabetics and overt diabetics were compared to matched controls.Results: No differences in EROD activity were observed among overt or gestational diabetics and their respectively matched controls. |
| 163 | 10838356 | Effects of gestational and overt diabetes on placental cytochromes P450 and glutathione S-transferase. |
| 164 | 10838356 | Objective: Animal and in vivo human studies have observed that diabetes alters the expression of hepatic metabolizing cytochrome P450 (CYP) and glutathione S-transferase (GST) enzymes. |
| 165 | 10838356 | Our objective was to compare placental xenobiotic metabolizing activity in diabetics to matched non-diabetic controls to determine if the presence of diabetes alters placental xenobiotic metabolizing activity.Methods: The catalytic activities of 7-ethoxyresorufin-O-deethylation [EROD] (CYP1A1), chlorzoxazone 6-hydroxylation (CYP2E1), dextromethorphan N-demethylation (CYP3A4), dextromethorphan O-demethylation (CYP2D6), and 1-chloro-2,4-dinitrobenzene (CDNB) conjugation with glutathione (GST) from placentas of diet controlled (class A1) and insulin-dependent (class A2) gestational diabetics and overt diabetics were compared to matched controls.Results: No differences in EROD activity were observed among overt or gestational diabetics and their respectively matched controls. |
| 166 | 10901185 | No association of glutathione S-transferase M1 gene polymorphism with diabetic nephropathy in Japanese type 2 diabetic patients. |
| 167 | 10901185 | The M1 member of GST mu class (GSTM1) is polymorphic and only expressed in 55-60% of Caucasians because of the homozygous deletion of the gene (null genotype). |
| 168 | 11865348 | With glutathione S-transferase (GST) as a measure of tubular damage, we now decide whether to transplant based on GST values. |
| 169 | 11894723 | In the evaluation of the carbohydrate metabolism in non-diabetic women, we found no effect on fasting glucose or insulin and no effect on the insulin response to oral glucose in women using monophasic OCs containing EE combined with DSG or GST. |
| 170 | 11894723 | In the women with IDDM there was a negative correlation between daily insulin requirement and HDL-cholesterol before and during treatment, but no other statistically significant correlation between estimates of glycaemic control and lipids and lipoproteins were observed. |
| 171 | 11894723 | In the non-diabetic women, changes in the haemostatic system included an increase in the procoagulant factors fibrinogen and Factor VIIc; the concentration of active t-PA increased, mainly because of decreased inhibition by PAI-1. |
| 172 | 11894723 | The regulation of the t-PA/PAI system was studied in non-diabetic women in order to elucidate if the effects of OCs are caused by a direct effect on synthesis or clearance of these variables or if they are secondary to changed insulin sensitivity, as described in individuals with atherosclerosis. |
| 173 | 11894723 | We found no indications that insulin resistance is involved in the regulation of t-PA and PAI-1 antigen levels, neither before nor during intake of OCs. |
| 174 | 11985890 | Polycyclic aromatic hydrocarbons (PAHs) and N-nitrosamines (NNA) are mainly activated by cytochrome P450s, and their associated enzyme activities such as aryl hydrocarbon (benzo(a)pyrene) hydroxylase (AHH), N-nitrosdimethylamine N-demethylase I (NDMA-dI), NADPH-cytochrome C reductase, and detoxified by glutathione S-transferase (GST) and glutathione (GSH). |
| 175 | 11985890 | Alloxan treatment increased the hepatic activity of cytochrome P450, NADPH-cytochrome C reductase, AHH, NDMA-dI, GST and GSH by 112, 122, 82, 99, 64 and 26%, respectively. |
| 176 | 11985890 | Polycyclic aromatic hydrocarbons (PAHs) and N-nitrosamines (NNA) are mainly activated by cytochrome P450s, and their associated enzyme activities such as aryl hydrocarbon (benzo(a)pyrene) hydroxylase (AHH), N-nitrosdimethylamine N-demethylase I (NDMA-dI), NADPH-cytochrome C reductase, and detoxified by glutathione S-transferase (GST) and glutathione (GSH). |
| 177 | 11985890 | Alloxan treatment increased the hepatic activity of cytochrome P450, NADPH-cytochrome C reductase, AHH, NDMA-dI, GST and GSH by 112, 122, 82, 99, 64 and 26%, respectively. |
| 178 | 12002418 | In the renal cortex of rats with streptozotocin-induced diabetes, the activity of superoxide dismutase (SOD) isoenzymes, glutathione peroxidase (GSH-Pox). glutathione S-transferase (GST) and glutathione reductase (GSH-RED) was measured in the 5th, 10th and 15th weeks of diabetes. |
| 179 | 12355813 | [Glutathione S-transferase (GST)]. |
| 180 | 12453887 | Identification of the insulin-regulated interaction of phosphodiesterase 3B with 14-3-3 beta protein. |
| 181 | 12453887 | Insulin-induced phosphorylation and activation of PDE3B is phosphatidylinositol 3-kinase (PI3-K) and Akt dependent, but the precise mechanism of PDE3B activation is not fully understood. |
| 182 | 12453887 | The glutathione S-transferase (GST)-tagged 14-3-3 beta interacts with endogenous PDE3B of rat adipocytes, and this interaction is enhanced when adipocytes are treated with insulin. |
| 183 | 12453887 | Synthetic 15 amino acid peptides of rat PDE3B containing phosphorylated Ser-279 or -302 inhibit this interaction, indicating that the insulin-regulated phosphorylation of these serine residues is involved. |
| 184 | 12453887 | Because insulin receptor substrate-1 also associates with 14-3-3, the dimeric 14-3-3 beta could function as a scaffolding protein in the activation of PDE3B by insulin. |
| 185 | 12592416 | Simultaneous determination of glutathione S-transferase (GST), selenium dependent glutathione peroxidase (Se-GPx), catalase (CAT) activities and thiobarbituric acid reactive-substances (TBARs) levels were carried out in maternal erythrocyte and plasma in the antenatal period (in the third trimester) and immediately after the delivery. |
| 186 | 12592416 | Erythrocyte GST activity was significantly increased in insulin-dependent diabetic pregnancy (IDDP) when compared to the control (P<0.05). |
| 187 | 12592416 | Simultaneous determination of glutathione S-transferase (GST), selenium dependent glutathione peroxidase (Se-GPx), catalase (CAT) activities and thiobarbituric acid reactive-substances (TBARs) levels were carried out in maternal erythrocyte and plasma in the antenatal period (in the third trimester) and immediately after the delivery. |
| 188 | 12592416 | Erythrocyte GST activity was significantly increased in insulin-dependent diabetic pregnancy (IDDP) when compared to the control (P<0.05). |
| 189 | 12649389 | Insulin and glucagon regulation of glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 190 | 12649389 | Insulin and glucagon effects on GST expression and the signaling pathway involved in the glucagon regulation of GST expression were examined in primary cultured rat hepatocytes. |
| 191 | 12649389 | The addition of insulin resulted in the elevation of alpha-class GST protein levels, whereas alpha- and pi-class GST protein levels were markedly decreased in hepatocytes cultured with glucagon. |
| 192 | 12649389 | In contrast, mu-class GST protein expression was unaffected by insulin or glucagon treatment. |
| 193 | 12649389 | Insulin concentrations >/=1 nM resulted in increased GST activities and alpha-class GST protein levels, whereas glucagon concentrations >/=20 nM decreased alpha- and pi-class protein levels and activity. |
| 194 | 12649389 | This study demonstrates that insulin and glucagon regulate, in an opposing manner, the expression of alpha-class GSTs and that glucagon completely inhibits pi-class GST expression in vitro, suggesting that hepatic GST expression may be decreased during diabetes. |
| 195 | 12649389 | Furthermore, the present study implicates cAMP and protein kinase A in mediating the inhibitory effect of glucagon on GST expression. |
| 196 | 12649389 | Insulin and glucagon regulation of glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 197 | 12649389 | Insulin and glucagon effects on GST expression and the signaling pathway involved in the glucagon regulation of GST expression were examined in primary cultured rat hepatocytes. |
| 198 | 12649389 | The addition of insulin resulted in the elevation of alpha-class GST protein levels, whereas alpha- and pi-class GST protein levels were markedly decreased in hepatocytes cultured with glucagon. |
| 199 | 12649389 | In contrast, mu-class GST protein expression was unaffected by insulin or glucagon treatment. |
| 200 | 12649389 | Insulin concentrations >/=1 nM resulted in increased GST activities and alpha-class GST protein levels, whereas glucagon concentrations >/=20 nM decreased alpha- and pi-class protein levels and activity. |
| 201 | 12649389 | This study demonstrates that insulin and glucagon regulate, in an opposing manner, the expression of alpha-class GSTs and that glucagon completely inhibits pi-class GST expression in vitro, suggesting that hepatic GST expression may be decreased during diabetes. |
| 202 | 12649389 | Furthermore, the present study implicates cAMP and protein kinase A in mediating the inhibitory effect of glucagon on GST expression. |
| 203 | 12649389 | Insulin and glucagon regulation of glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 204 | 12649389 | Insulin and glucagon effects on GST expression and the signaling pathway involved in the glucagon regulation of GST expression were examined in primary cultured rat hepatocytes. |
| 205 | 12649389 | The addition of insulin resulted in the elevation of alpha-class GST protein levels, whereas alpha- and pi-class GST protein levels were markedly decreased in hepatocytes cultured with glucagon. |
| 206 | 12649389 | In contrast, mu-class GST protein expression was unaffected by insulin or glucagon treatment. |
| 207 | 12649389 | Insulin concentrations >/=1 nM resulted in increased GST activities and alpha-class GST protein levels, whereas glucagon concentrations >/=20 nM decreased alpha- and pi-class protein levels and activity. |
| 208 | 12649389 | This study demonstrates that insulin and glucagon regulate, in an opposing manner, the expression of alpha-class GSTs and that glucagon completely inhibits pi-class GST expression in vitro, suggesting that hepatic GST expression may be decreased during diabetes. |
| 209 | 12649389 | Furthermore, the present study implicates cAMP and protein kinase A in mediating the inhibitory effect of glucagon on GST expression. |
| 210 | 12649389 | Insulin and glucagon regulation of glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 211 | 12649389 | Insulin and glucagon effects on GST expression and the signaling pathway involved in the glucagon regulation of GST expression were examined in primary cultured rat hepatocytes. |
| 212 | 12649389 | The addition of insulin resulted in the elevation of alpha-class GST protein levels, whereas alpha- and pi-class GST protein levels were markedly decreased in hepatocytes cultured with glucagon. |
| 213 | 12649389 | In contrast, mu-class GST protein expression was unaffected by insulin or glucagon treatment. |
| 214 | 12649389 | Insulin concentrations >/=1 nM resulted in increased GST activities and alpha-class GST protein levels, whereas glucagon concentrations >/=20 nM decreased alpha- and pi-class protein levels and activity. |
| 215 | 12649389 | This study demonstrates that insulin and glucagon regulate, in an opposing manner, the expression of alpha-class GSTs and that glucagon completely inhibits pi-class GST expression in vitro, suggesting that hepatic GST expression may be decreased during diabetes. |
| 216 | 12649389 | Furthermore, the present study implicates cAMP and protein kinase A in mediating the inhibitory effect of glucagon on GST expression. |
| 217 | 12649389 | Insulin and glucagon regulation of glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 218 | 12649389 | Insulin and glucagon effects on GST expression and the signaling pathway involved in the glucagon regulation of GST expression were examined in primary cultured rat hepatocytes. |
| 219 | 12649389 | The addition of insulin resulted in the elevation of alpha-class GST protein levels, whereas alpha- and pi-class GST protein levels were markedly decreased in hepatocytes cultured with glucagon. |
| 220 | 12649389 | In contrast, mu-class GST protein expression was unaffected by insulin or glucagon treatment. |
| 221 | 12649389 | Insulin concentrations >/=1 nM resulted in increased GST activities and alpha-class GST protein levels, whereas glucagon concentrations >/=20 nM decreased alpha- and pi-class protein levels and activity. |
| 222 | 12649389 | This study demonstrates that insulin and glucagon regulate, in an opposing manner, the expression of alpha-class GSTs and that glucagon completely inhibits pi-class GST expression in vitro, suggesting that hepatic GST expression may be decreased during diabetes. |
| 223 | 12649389 | Furthermore, the present study implicates cAMP and protein kinase A in mediating the inhibitory effect of glucagon on GST expression. |
| 224 | 12649389 | Insulin and glucagon regulation of glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 225 | 12649389 | Insulin and glucagon effects on GST expression and the signaling pathway involved in the glucagon regulation of GST expression were examined in primary cultured rat hepatocytes. |
| 226 | 12649389 | The addition of insulin resulted in the elevation of alpha-class GST protein levels, whereas alpha- and pi-class GST protein levels were markedly decreased in hepatocytes cultured with glucagon. |
| 227 | 12649389 | In contrast, mu-class GST protein expression was unaffected by insulin or glucagon treatment. |
| 228 | 12649389 | Insulin concentrations >/=1 nM resulted in increased GST activities and alpha-class GST protein levels, whereas glucagon concentrations >/=20 nM decreased alpha- and pi-class protein levels and activity. |
| 229 | 12649389 | This study demonstrates that insulin and glucagon regulate, in an opposing manner, the expression of alpha-class GSTs and that glucagon completely inhibits pi-class GST expression in vitro, suggesting that hepatic GST expression may be decreased during diabetes. |
| 230 | 12649389 | Furthermore, the present study implicates cAMP and protein kinase A in mediating the inhibitory effect of glucagon on GST expression. |
| 231 | 12682826 | To address these issues, a C-terminus regulatory domain of NHE-1 was cloned and sequenced from normal human placentas, and was used to prepare a GST-fusion protein for raising polyclonal antibodies. |
| 232 | 12682826 | The level of NHE-1 protein was decreased significantly ( p<0.05) in diabetic placentas, whereas beta-actin, an internal control, remained unaltered. |
| 233 | 12682826 | Interestingly, the levels of NHE-1 mRNA and beta-actin mRNA did not change in diabetic pregnancies. |
| 234 | 12718433 | In the brain, although 6-phosphogluconate dehydrogenase activity (6-PGD) did not change, glucose-6-phosphate dehydrogenase activity (G-6PD) was markedly increased in diabetic rats compared with controls; only combined treatment with ST and vitamin E produced a partial prevention on this alteration. |
| 235 | 12718433 | The aorta G-6PD and 6-PGD of diabetic rats were 52% and 36% of control values, respectively. |
| 236 | 12718433 | Neither single treatments with each antioxidant nor their combination altered the G-6PD and 6-PGD in aorta of diabetic rats. |
| 237 | 12718433 | Glutathione S-transferase (GST) activity did not significantly change in diabetic brain and aorta. |
| 238 | 12853069 | The extent of lipid peroxidation (LPO) and antioxidant defense system [i.e., levels of glutathione (GSH), glucose-6-phosphate dehydrogenase (G6PDH), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and catalase (CAT)] were evaluated in reticulocytes and erythrocytes of type 2 diabetic males and age-matched controls. |
| 239 | 12853069 | Type 2 diabetics have shown increased lipid peroxidation and decreased levels of GSH, GR, GPx, G6PDH, and GST both in reticulocytes and erythrocytes compared to controls, indicating the presence of oxidative stress and defective antioxidant systems in these patients. |
| 240 | 12853069 | The extent of lipid peroxidation (LPO) and antioxidant defense system [i.e., levels of glutathione (GSH), glucose-6-phosphate dehydrogenase (G6PDH), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and catalase (CAT)] were evaluated in reticulocytes and erythrocytes of type 2 diabetic males and age-matched controls. |
| 241 | 12853069 | Type 2 diabetics have shown increased lipid peroxidation and decreased levels of GSH, GR, GPx, G6PDH, and GST both in reticulocytes and erythrocytes compared to controls, indicating the presence of oxidative stress and defective antioxidant systems in these patients. |
| 242 | 12890544 | Concomitantly, significant decreases in the levels of antioxidants ceruloplasmin, albumin and total thiols were found in the plasma of diabetic rats. |
| 243 | 12890544 | In erythrocytes lysate, glutathione S-transferase (GST) activities were increased significantly in rats treated with garlic oil or melatonin, while lipid peroxides decreased significantly and total thiol increased significantly in melatonin or garlic oil treatment, respectively. |
| 244 | 12890544 | In liver homogenates of rats treated with garlic or melatonin, lipid peroxides were decreased significantly, and GST activities increased significantly, while SOD activities were increased significantly in liver and kidney after garlic or melatonin treatment. |
| 245 | 12890544 | Concomitantly, significant decreases in the levels of antioxidants ceruloplasmin, albumin and total thiols were found in the plasma of diabetic rats. |
| 246 | 12890544 | In erythrocytes lysate, glutathione S-transferase (GST) activities were increased significantly in rats treated with garlic oil or melatonin, while lipid peroxides decreased significantly and total thiol increased significantly in melatonin or garlic oil treatment, respectively. |
| 247 | 12890544 | In liver homogenates of rats treated with garlic or melatonin, lipid peroxides were decreased significantly, and GST activities increased significantly, while SOD activities were increased significantly in liver and kidney after garlic or melatonin treatment. |
| 248 | 14692396 | The IDDM and NIDDM patients had above-normal absolute lymphocyte counts, whereas the percentages of CD3, CD4 adn CD8 T lymphocytes were significantly reduced. |
| 249 | 14692396 | The low intracellular reduced glutathione(GSH) and the unbalanced profile of key enzymes involved in GSH metabolism, gamma-glutamyltransferase (gamma-GT) and glutathione-S-transferase (GST), account for the increased oxidative status of PBMC from diabetic patients. |
| 250 | 14693714 | Elevated mitochondrial cytochrome P450 2E1 and glutathione S-transferase A4-4 in streptozotocin-induced diabetic rats: tissue-specific variations and roles in oxidative stress. |
| 251 | 14693714 | We show a five- to eightfold increase of cytochrome P450 2E1 (CYP2E1) and glutathione S-transferase (GST) A4-4 levels in mitochondria from STZ-treated rat tissues compared with those in nondiabetic rat tissues, suggesting possible roles in the disease process. |
| 252 | 14693714 | Transient transfection of COS cells with CYP2E1 cDNA caused a similar accumulation of CYP2E1 and GST A4-4 in mitochondria and increased production of mitochondrial ROS. |
| 253 | 14693714 | Elevated mitochondrial cytochrome P450 2E1 and glutathione S-transferase A4-4 in streptozotocin-induced diabetic rats: tissue-specific variations and roles in oxidative stress. |
| 254 | 14693714 | We show a five- to eightfold increase of cytochrome P450 2E1 (CYP2E1) and glutathione S-transferase (GST) A4-4 levels in mitochondria from STZ-treated rat tissues compared with those in nondiabetic rat tissues, suggesting possible roles in the disease process. |
| 255 | 14693714 | Transient transfection of COS cells with CYP2E1 cDNA caused a similar accumulation of CYP2E1 and GST A4-4 in mitochondria and increased production of mitochondrial ROS. |
| 256 | 14729399 | Here, we demonstrate by immunohistochemistry, that glutathione S-transferase (GST) isoenzymes are differentially expressed in the liver, kidney and testis of diabetic rats. |
| 257 | 15064821 | The diabetic control rats (N = 6) presented a significant increase in blood glucose, sorbitol dehydrogenase, glycosylated hemoglobin and lipid peroxidation markers such as thiobarbituric acid reactive substances (TBARS) and hydroperoxides, and a significant decrease in plasma insulin and antioxidant enzymes such as glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) compared to normal rats (N = 6). |
| 258 | 15064821 | Scoparia dulcis plant extract (SPEt, 200 mg kg-1 day-1) and glibenclamide (600 microg kg-1 day-1), a reference drug, were administered by gavage for 6 weeks to diabetic rats (N = 6 for each group) and significantly reduced blood glucose, sorbitol dehydrogenase, glycosylated hemoglobin, TBARS, and hydroperoxides, and significantly increased plasma insulin, GPx, GST and GSH activities in liver. |
| 259 | 15064821 | The effect of the extract may have been due to the decreased influx of glucose into the polyol pathway leading to increased activities of antioxidant enzymes and plasma insulin and decreased activity of sorbitol dehydrogenase. |
| 260 | 15064821 | The diabetic control rats (N = 6) presented a significant increase in blood glucose, sorbitol dehydrogenase, glycosylated hemoglobin and lipid peroxidation markers such as thiobarbituric acid reactive substances (TBARS) and hydroperoxides, and a significant decrease in plasma insulin and antioxidant enzymes such as glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) compared to normal rats (N = 6). |
| 261 | 15064821 | Scoparia dulcis plant extract (SPEt, 200 mg kg-1 day-1) and glibenclamide (600 microg kg-1 day-1), a reference drug, were administered by gavage for 6 weeks to diabetic rats (N = 6 for each group) and significantly reduced blood glucose, sorbitol dehydrogenase, glycosylated hemoglobin, TBARS, and hydroperoxides, and significantly increased plasma insulin, GPx, GST and GSH activities in liver. |
| 262 | 15064821 | The effect of the extract may have been due to the decreased influx of glucose into the polyol pathway leading to increased activities of antioxidant enzymes and plasma insulin and decreased activity of sorbitol dehydrogenase. |
| 263 | 15249052 | We report here the development of a method for high-level expression and purification of recombinant hGLP-1 (7-36) amide (rhGLP-1) through glutathione S-transferase (GST) fusion expression system. |
| 264 | 15249052 | Following cleavage of GST-hGLP-1-Leu by cyanogen bromide, the recombinant hGLP-1-Leu was released from fusion protein, and purified using QAE Sepharose ion exchange and RP C(18) chromatography. |
| 265 | 15249052 | We report here the development of a method for high-level expression and purification of recombinant hGLP-1 (7-36) amide (rhGLP-1) through glutathione S-transferase (GST) fusion expression system. |
| 266 | 15249052 | Following cleavage of GST-hGLP-1-Leu by cyanogen bromide, the recombinant hGLP-1-Leu was released from fusion protein, and purified using QAE Sepharose ion exchange and RP C(18) chromatography. |
| 267 | 15286406 | The following enzymes were measured - hexokinase (HK), glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), glutathione-s-transferase (GST), alanine aminotransferase (AlaAT), aspartate aminotransferase (AsAT) and arginase in the hemolysates of all the RBCs fractions. |
| 268 | 15900084 | The decrease in thiobarbituric acid reactive substances (TBARS) and hydroperoxides (HPX) and increase in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH) and glutathione-S-transferase (GST) clearly show the antioxidant properties of SPEt in addition to its antidiabetic effect. |
| 269 | 15907058 | Glucose, urea and glutathione-S-transferase (GST) in plasma, glutathione (GSH) and malondialdehyde (MDA) levels in erythrocytes were estimated in all the groups at the end of four weeks. |
| 270 | 16037268 | The results showed that: (1) fructoselysine was observed in the hepatic portal veins, arteries, and femoral veins of rats fed with glycated proteins after 2 h of feeding; (2) blood sugar of glycated protein-fed rats was lower than that of diabetic rats fed with intact protein, while HbA1C in blood and glucose in urine of both groups were similar; (3) lipid peroxidation status in serum, liver, and kidney of both groups was similar; (4) superoxide dismutase (SOD) and glutathione-S-transferase (GST) enzymatic activity in serum and liver of both groups were also similar; (5) there were no differences in degree of cataract formation and concentration of glucose, fructose, sorbitol, and lipid peroxide in the lenses of both groups. |
| 271 | 16173921 | Glucokinase acts as the pancreatic glucose sensor and plays a critical role in the regulation of insulin secretion by the beta-cell. |
| 272 | 16173921 | We have identified and functionally characterized missense mutations in the GCK gene in diabetic families that result in protein mutations Leu165-->Phe, Glu265-->Lys and Thr206-->Met. |
| 273 | 16173921 | In order to measure the biochemical effects of these missense mutations on glucokinase activity, we bacterially expressed and affinity-purified islet human glucokinase proteins carrying the respective mutations and fused to GST (glutathione S-transferase). |
| 274 | 16173921 | Enzymatic assays on the recombinant proteins revealed that mutations Thr206-->Met and Leu165-->Phe strongly affect the kinetic parameters of glucokinase, in agreement with the localization of both residues close to the active site of the enzyme. |
| 275 | 16289604 | The treatment with HAEt significantly increased the glutathione (GSH), glutathione peroxidase (GPx), glutathione S-transferase (GST) and catalase (CAT) in the drug-treated group, which is comparable to the control group. |
| 276 | 16293713 | Identification of the insulin signaling cascade in the regulation of alpha-class glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 277 | 16293713 | We reported previously that insulin elevated alpha-class glutathione S-transferase (GSTs) protein levels in primary cultured rat hepatocytes (Kim et al., 2003b). |
| 278 | 16293713 | In contrast, glucagon down-regulated alpha- and pi-class GST expression, and mechanistic research implicated cAMP and protein kinase A in this process (Kim et al., 2003b). |
| 279 | 16293713 | The present study examines the signaling pathways involved in the regulation of alpha-class GST in response to insulin in primary cultured rat hepatocytes. |
| 280 | 16293713 | Protein levels of GSTA1/2 and GSTA3/5 and activity of GST toward 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole (NBD) were increased in an insulin concentration-dependent manner. |
| 281 | 16293713 | Treatment of cells with the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one] or rapamycin, an inhibitor of mammalian target of rapamycin and ribosomal p70 S6 kinase (p70S6K) phosphorylation, or with an adenovirus containing green fluorescent protein and a dominant-negative and kinase-dead Akt, effectively inhibited the insulin-mediated increase in alpha-class GST expression and GST activity toward NBD. |
| 282 | 16293713 | In contrast, PD98059 (2'-amino-3'-methoxyflavone), an inhibitor of mitogen-activated protein kinase kinase, SP600125 (1,9-pyrazoloanthrone), an inhibitor of c-Jun N-terminal kinase, SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imadazole], an inhibitor of p38 mitogen-activated protein kinase, or bisindolylmaleimide, a broad spectrum inhibitor of protein kinase C, did not inhibit the insulin-mediated increase in alpha-class GST protein levels in hepatocytes. |
| 283 | 16293713 | These results show that PI3K/Akt/p70S6K signaling is active in the insulin-mediated up-regulation of the antioxidant defense system and that low insulin levels, as encountered in diabetes, potentially increase the susceptibility of hepatocytes to xenobiotic-mediated and/or oxidative stress-mediated damage. |
| 284 | 16293713 | Identification of the insulin signaling cascade in the regulation of alpha-class glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 285 | 16293713 | We reported previously that insulin elevated alpha-class glutathione S-transferase (GSTs) protein levels in primary cultured rat hepatocytes (Kim et al., 2003b). |
| 286 | 16293713 | In contrast, glucagon down-regulated alpha- and pi-class GST expression, and mechanistic research implicated cAMP and protein kinase A in this process (Kim et al., 2003b). |
| 287 | 16293713 | The present study examines the signaling pathways involved in the regulation of alpha-class GST in response to insulin in primary cultured rat hepatocytes. |
| 288 | 16293713 | Protein levels of GSTA1/2 and GSTA3/5 and activity of GST toward 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole (NBD) were increased in an insulin concentration-dependent manner. |
| 289 | 16293713 | Treatment of cells with the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one] or rapamycin, an inhibitor of mammalian target of rapamycin and ribosomal p70 S6 kinase (p70S6K) phosphorylation, or with an adenovirus containing green fluorescent protein and a dominant-negative and kinase-dead Akt, effectively inhibited the insulin-mediated increase in alpha-class GST expression and GST activity toward NBD. |
| 290 | 16293713 | In contrast, PD98059 (2'-amino-3'-methoxyflavone), an inhibitor of mitogen-activated protein kinase kinase, SP600125 (1,9-pyrazoloanthrone), an inhibitor of c-Jun N-terminal kinase, SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imadazole], an inhibitor of p38 mitogen-activated protein kinase, or bisindolylmaleimide, a broad spectrum inhibitor of protein kinase C, did not inhibit the insulin-mediated increase in alpha-class GST protein levels in hepatocytes. |
| 291 | 16293713 | These results show that PI3K/Akt/p70S6K signaling is active in the insulin-mediated up-regulation of the antioxidant defense system and that low insulin levels, as encountered in diabetes, potentially increase the susceptibility of hepatocytes to xenobiotic-mediated and/or oxidative stress-mediated damage. |
| 292 | 16293713 | Identification of the insulin signaling cascade in the regulation of alpha-class glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 293 | 16293713 | We reported previously that insulin elevated alpha-class glutathione S-transferase (GSTs) protein levels in primary cultured rat hepatocytes (Kim et al., 2003b). |
| 294 | 16293713 | In contrast, glucagon down-regulated alpha- and pi-class GST expression, and mechanistic research implicated cAMP and protein kinase A in this process (Kim et al., 2003b). |
| 295 | 16293713 | The present study examines the signaling pathways involved in the regulation of alpha-class GST in response to insulin in primary cultured rat hepatocytes. |
| 296 | 16293713 | Protein levels of GSTA1/2 and GSTA3/5 and activity of GST toward 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole (NBD) were increased in an insulin concentration-dependent manner. |
| 297 | 16293713 | Treatment of cells with the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one] or rapamycin, an inhibitor of mammalian target of rapamycin and ribosomal p70 S6 kinase (p70S6K) phosphorylation, or with an adenovirus containing green fluorescent protein and a dominant-negative and kinase-dead Akt, effectively inhibited the insulin-mediated increase in alpha-class GST expression and GST activity toward NBD. |
| 298 | 16293713 | In contrast, PD98059 (2'-amino-3'-methoxyflavone), an inhibitor of mitogen-activated protein kinase kinase, SP600125 (1,9-pyrazoloanthrone), an inhibitor of c-Jun N-terminal kinase, SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imadazole], an inhibitor of p38 mitogen-activated protein kinase, or bisindolylmaleimide, a broad spectrum inhibitor of protein kinase C, did not inhibit the insulin-mediated increase in alpha-class GST protein levels in hepatocytes. |
| 299 | 16293713 | These results show that PI3K/Akt/p70S6K signaling is active in the insulin-mediated up-regulation of the antioxidant defense system and that low insulin levels, as encountered in diabetes, potentially increase the susceptibility of hepatocytes to xenobiotic-mediated and/or oxidative stress-mediated damage. |
| 300 | 16293713 | Identification of the insulin signaling cascade in the regulation of alpha-class glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 301 | 16293713 | We reported previously that insulin elevated alpha-class glutathione S-transferase (GSTs) protein levels in primary cultured rat hepatocytes (Kim et al., 2003b). |
| 302 | 16293713 | In contrast, glucagon down-regulated alpha- and pi-class GST expression, and mechanistic research implicated cAMP and protein kinase A in this process (Kim et al., 2003b). |
| 303 | 16293713 | The present study examines the signaling pathways involved in the regulation of alpha-class GST in response to insulin in primary cultured rat hepatocytes. |
| 304 | 16293713 | Protein levels of GSTA1/2 and GSTA3/5 and activity of GST toward 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole (NBD) were increased in an insulin concentration-dependent manner. |
| 305 | 16293713 | Treatment of cells with the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one] or rapamycin, an inhibitor of mammalian target of rapamycin and ribosomal p70 S6 kinase (p70S6K) phosphorylation, or with an adenovirus containing green fluorescent protein and a dominant-negative and kinase-dead Akt, effectively inhibited the insulin-mediated increase in alpha-class GST expression and GST activity toward NBD. |
| 306 | 16293713 | In contrast, PD98059 (2'-amino-3'-methoxyflavone), an inhibitor of mitogen-activated protein kinase kinase, SP600125 (1,9-pyrazoloanthrone), an inhibitor of c-Jun N-terminal kinase, SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imadazole], an inhibitor of p38 mitogen-activated protein kinase, or bisindolylmaleimide, a broad spectrum inhibitor of protein kinase C, did not inhibit the insulin-mediated increase in alpha-class GST protein levels in hepatocytes. |
| 307 | 16293713 | These results show that PI3K/Akt/p70S6K signaling is active in the insulin-mediated up-regulation of the antioxidant defense system and that low insulin levels, as encountered in diabetes, potentially increase the susceptibility of hepatocytes to xenobiotic-mediated and/or oxidative stress-mediated damage. |
| 308 | 16293713 | Identification of the insulin signaling cascade in the regulation of alpha-class glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 309 | 16293713 | We reported previously that insulin elevated alpha-class glutathione S-transferase (GSTs) protein levels in primary cultured rat hepatocytes (Kim et al., 2003b). |
| 310 | 16293713 | In contrast, glucagon down-regulated alpha- and pi-class GST expression, and mechanistic research implicated cAMP and protein kinase A in this process (Kim et al., 2003b). |
| 311 | 16293713 | The present study examines the signaling pathways involved in the regulation of alpha-class GST in response to insulin in primary cultured rat hepatocytes. |
| 312 | 16293713 | Protein levels of GSTA1/2 and GSTA3/5 and activity of GST toward 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole (NBD) were increased in an insulin concentration-dependent manner. |
| 313 | 16293713 | Treatment of cells with the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one] or rapamycin, an inhibitor of mammalian target of rapamycin and ribosomal p70 S6 kinase (p70S6K) phosphorylation, or with an adenovirus containing green fluorescent protein and a dominant-negative and kinase-dead Akt, effectively inhibited the insulin-mediated increase in alpha-class GST expression and GST activity toward NBD. |
| 314 | 16293713 | In contrast, PD98059 (2'-amino-3'-methoxyflavone), an inhibitor of mitogen-activated protein kinase kinase, SP600125 (1,9-pyrazoloanthrone), an inhibitor of c-Jun N-terminal kinase, SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imadazole], an inhibitor of p38 mitogen-activated protein kinase, or bisindolylmaleimide, a broad spectrum inhibitor of protein kinase C, did not inhibit the insulin-mediated increase in alpha-class GST protein levels in hepatocytes. |
| 315 | 16293713 | These results show that PI3K/Akt/p70S6K signaling is active in the insulin-mediated up-regulation of the antioxidant defense system and that low insulin levels, as encountered in diabetes, potentially increase the susceptibility of hepatocytes to xenobiotic-mediated and/or oxidative stress-mediated damage. |
| 316 | 16293713 | Identification of the insulin signaling cascade in the regulation of alpha-class glutathione S-transferase expression in primary cultured rat hepatocytes. |
| 317 | 16293713 | We reported previously that insulin elevated alpha-class glutathione S-transferase (GSTs) protein levels in primary cultured rat hepatocytes (Kim et al., 2003b). |
| 318 | 16293713 | In contrast, glucagon down-regulated alpha- and pi-class GST expression, and mechanistic research implicated cAMP and protein kinase A in this process (Kim et al., 2003b). |
| 319 | 16293713 | The present study examines the signaling pathways involved in the regulation of alpha-class GST in response to insulin in primary cultured rat hepatocytes. |
| 320 | 16293713 | Protein levels of GSTA1/2 and GSTA3/5 and activity of GST toward 7-chloro-4-nitrobenzo-2-oxa-1,3-diazole (NBD) were increased in an insulin concentration-dependent manner. |
| 321 | 16293713 | Treatment of cells with the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one] or rapamycin, an inhibitor of mammalian target of rapamycin and ribosomal p70 S6 kinase (p70S6K) phosphorylation, or with an adenovirus containing green fluorescent protein and a dominant-negative and kinase-dead Akt, effectively inhibited the insulin-mediated increase in alpha-class GST expression and GST activity toward NBD. |
| 322 | 16293713 | In contrast, PD98059 (2'-amino-3'-methoxyflavone), an inhibitor of mitogen-activated protein kinase kinase, SP600125 (1,9-pyrazoloanthrone), an inhibitor of c-Jun N-terminal kinase, SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imadazole], an inhibitor of p38 mitogen-activated protein kinase, or bisindolylmaleimide, a broad spectrum inhibitor of protein kinase C, did not inhibit the insulin-mediated increase in alpha-class GST protein levels in hepatocytes. |
| 323 | 16293713 | These results show that PI3K/Akt/p70S6K signaling is active in the insulin-mediated up-regulation of the antioxidant defense system and that low insulin levels, as encountered in diabetes, potentially increase the susceptibility of hepatocytes to xenobiotic-mediated and/or oxidative stress-mediated damage. |
| 324 | 16293776 | We previously identified Bridge-1 (PSMD9) as a PDZ-domain coregulator that augments insulin gene transcription via interactions with the basic helix-loop-helix transcription factors E12 and E47, and that increases transcriptional activation by the homeodomain transcription factor PDX-1. |
| 325 | 16293776 | In these studies, we find that transcriptional activation by Bridge-1 can be regulated via interactions with the histone acetyltransferase and nuclear receptor coactivator p300. |
| 326 | 16293776 | We demonstrate that p300 and Bridge-1 proteins interact in immunopre-cipitation and glutathione-S-transferase (GST) pull-down assays. |
| 327 | 16293776 | Bridge-1 interacts directly with multiple regions within p300 that encompass C/H1 or C/H2 cysteine- and histidine-rich protein interaction domains and the histone acetyltransferase domain. |
| 328 | 16325418 | Production of a truncated soluble human semicarbazide-sensitive amine oxidase mediated by a GST-fusion protein secreted from HEK293 cells. |
| 329 | 16325418 | Elevated levels of semicarbazide-sensitive amine oxidase (SSAO) activity have been observed in several human conditions such as congestive heart failure, diabetes mellitus, and inflammation. |
| 330 | 16325418 | The extracellular region (residues 29-763) of human SSAO was expressed in HEK293 cells in fusion with a mutated Schistosoma japonicum glutathione S-transferase (GST) and secreted to the culture medium. |
| 331 | 16325418 | Production of a truncated soluble human semicarbazide-sensitive amine oxidase mediated by a GST-fusion protein secreted from HEK293 cells. |
| 332 | 16325418 | Elevated levels of semicarbazide-sensitive amine oxidase (SSAO) activity have been observed in several human conditions such as congestive heart failure, diabetes mellitus, and inflammation. |
| 333 | 16325418 | The extracellular region (residues 29-763) of human SSAO was expressed in HEK293 cells in fusion with a mutated Schistosoma japonicum glutathione S-transferase (GST) and secreted to the culture medium. |
| 334 | 16390810 | Glutathione-s-transferase M1 and T1 polymorphisms and associations with type 1 diabetes age-at-onset. |
| 335 | 16390810 | Glutathione-s-transferase mu 1 (GSTM1) and glutathione-s-transferase theta 1 (GSTT1) have polymorphic homozygous deletion (null) genotypes resulting in complete absence of enzyme activity. |
| 336 | 16390810 | GSTM1 and GSTT1 null genotypes in Caucasian populations have frequencies of approximately 40-60% and 15-20%, respectively. |
| 337 | 16390810 | The aim of this study was to investigate associations with GSTM1 and GSTT1 polymorphisms in a group T1D patients and control subjects 0-35 years old who participated in the Combined Swedish Childhood Diabetes Registry and Diabetes Incidence Study (1986-1988). |
| 338 | 16390810 | These results suggest that the GSTM1 null genotype is associated with T1D protection and T1D age-at-onset and that susceptibility to T1D may involve GST conjugation. |
| 339 | 16569213 | Angiotensin II stimulates phosphorylation of an ectodomain-truncated platelet-derived growth factor receptor-beta and its binding to class IA PI3K in vascular smooth muscle cells. |
| 340 | 16569213 | PI3K (phosphoinositide 3-kinase) activity is involved in Ang (angiotensin) II-stimulated VSMC (vascular smooth muscle cell) growth and hypertrophy. |
| 341 | 16569213 | In the present study, we demonstrate that the inhibition of PI3K in VSMCs by expression of a dominant-negative p85alpha mutant lacking the p110-binding domain (Deltap85), or by treatment of cells with LY294002, inhibited Ang II-stimulated PAI-1 (plasminogen activator inhibitor-1) mRNA expression. |
| 342 | 16569213 | Using a GST (glutathione S-transferase) fusion protein containing the p85 N-terminal SH2 (Src homology 2) domain as 'bait' followed by MS/MS (tandem MS), we identified a 70 kDa fragment of the p70 PDGFR-beta (platelet-derived growth factor receptor-beta) as a signalling adapter that is phosphorylated and recruits the p85 subunit of PI3K after Ang II stimulation of AT1 (Ang II subtype 1) receptors on VSMCs. |
| 343 | 16569213 | Stimulation of VSMCs with Ang II increased tyrosine-phosphorylation of p70 PDGFR-beta at Tyr751 and Tyr1021 and increased its binding to p85. |
| 344 | 16569213 | PDGF also induced phosphorylation of p70 PDGFR-beta, a response inhibited by the PDGF tyrosine kinase selective inhibitor, AG1296. |
| 345 | 16569213 | Ang II-stimulated phosphorylation of the p70 PDGFR-beta was blocked by the AT1 receptor antagonist, candesartan (CV 11974) and was partially inhibited by PP2 {4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine}, an Src family kinase inhibitor. |
| 346 | 16569213 | Our result suggests that the p70 PDGFR-beta functions as an adapter that recruits PI3K to the membrane upon AT1 receptor stimulation. |
| 347 | 16704309 | When in complex with fatty acids, FABP4 interacts with and modulates the activity of two important regulators of metabolism: hormone-sensitive lipase and peroxisome proliferator-activated receptor gamma. |
| 348 | 16704309 | Recombinant glutathione S-transferase (GST)-FABP4 or His-FABP4 was expressed in bacteria, affinity purified, and used for immunization of mice, enzyme-linked immunosorbent assay (ELISA) screening, and characterization of selected clones. |
| 349 | 16815474 | The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST). |
| 350 | 16815474 | The long-term hyperglycemia resulted in decreased activities of GSHPx (by 26%), catalase (by 34%), GST (by 38%) and G6PDH (by 27%) in diabetic animals. |
| 351 | 16815474 | The long-term ASA administration partially reversed the decrease in GSHPx activity, but did not influence the activities of catalase and GST in diabetic rats. |
| 352 | 16815474 | The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST). |
| 353 | 16815474 | The long-term hyperglycemia resulted in decreased activities of GSHPx (by 26%), catalase (by 34%), GST (by 38%) and G6PDH (by 27%) in diabetic animals. |
| 354 | 16815474 | The long-term ASA administration partially reversed the decrease in GSHPx activity, but did not influence the activities of catalase and GST in diabetic rats. |
| 355 | 16815474 | The aim of the present work was to investigate the effect of long-term ASA administration in experimental diabetes on activities of some liver enzymes: glutathione peroxidase (GSHPx), catalase, glucose-6-phosphate dehydrogenase (G6PDH) and glutathione S-transferase (GST). |
| 356 | 16815474 | The long-term hyperglycemia resulted in decreased activities of GSHPx (by 26%), catalase (by 34%), GST (by 38%) and G6PDH (by 27%) in diabetic animals. |
| 357 | 16815474 | The long-term ASA administration partially reversed the decrease in GSHPx activity, but did not influence the activities of catalase and GST in diabetic rats. |
| 358 | 16910316 | Plasma glucose, plasma insulin, thiobarbituricacid reactive substances (TBARS), hydroperoxides, superoxide dismutase (SOD), catalase (CAT), glutathione peroxide (Gpx), reduced glutathione (GSH), glutathione-S-transferase (GST), and vitamins C and E were assayed in liver and kidney. |
| 359 | 16910316 | In addition, the treated groups also showed a significant increase in the activities of plasma insulin, SOD, CAT, GPx, GST, GSH, vitamin C, and vitamin E in liver and kidney of STZ-nicotinamide-induced diabetic rats. |
| 360 | 16910316 | Plasma glucose, plasma insulin, thiobarbituricacid reactive substances (TBARS), hydroperoxides, superoxide dismutase (SOD), catalase (CAT), glutathione peroxide (Gpx), reduced glutathione (GSH), glutathione-S-transferase (GST), and vitamins C and E were assayed in liver and kidney. |
| 361 | 16910316 | In addition, the treated groups also showed a significant increase in the activities of plasma insulin, SOD, CAT, GPx, GST, GSH, vitamin C, and vitamin E in liver and kidney of STZ-nicotinamide-induced diabetic rats. |
| 362 | 16927413 | In the present study, we investigated the GSTM1, GSTT1 and GSTP1 gene polymorphisms in diabetic patients and healthy individuals and searched whether polymorphisms in GST genes are associated with diabetes mellitus (DM) in the Turkish population. |
| 363 | 16927413 | Genotyping of GSTM1, GSTT1 and GSTP1 genes was performed using real time polymerase chain reaction with a Light Cycler instrument. |
| 364 | 16927413 | However, there was no significant difference in the frequencies of the GSTT1 and GSTP1 gene polymorphisms between the patients and control group. |
| 365 | 17097148 | Our laboratory has reported that insulin and growth factors regulate drug metabolizing enzyme gene and protein expression, including cytochromes P450 (CYP), glutathione S-transferases (GST) and microsomal epoxide hydrolase (mEH), through receptors which are members of the large receptor tyrosine kinase (RTK) family, and by downstream effectors such as phosphatidylinositol 3-kinase, mitogen activated protein kinase (MAPK), Akt/protein kinase B (PKB), mammalian target of rapamycin (mTOR), and the p70 ribosomal protein S6 kinase (p70S6 kinase). |
| 366 | 17193903 | Activities of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glutathione S transferase (GST) were assessed in diabetic as well as rats co-administered with ALL. |
| 367 | 17211564 | The effect of the sulfonylurea glyburide on glutathione-S-transferase and glucose-6-phosphate dehydrogenase in streptozotocin-induced diabetic rat liver. |
| 368 | 17211564 | Glutathione-S-transferase (GST) catalyses the conjugation of glutathione with a variety of organic peroxides to form more water-soluble compounds. |
| 369 | 17211564 | Glucose-6-phosphate dehydrogenase (G6PDH) is essential to control intracellular reductive potential by increasing glutathione intracellular levels, which in turn decrease the amount of reactive oxygen species. |
| 370 | 17211564 | We investigated the activities of GST and G6PDH in the liver of both control and streptozotocin-induced diabetic rats. |
| 371 | 17211564 | Liver GST and G6PDH activities decreased significantly in five-week diabetic rats (p<0.001 and p<0.001 respectively) compared to controls and glyburide therapy restored these activities (p<0.001 for GST and p<0.001 for G6PDH). |
| 372 | 17211564 | The effect of the sulfonylurea glyburide on glutathione-S-transferase and glucose-6-phosphate dehydrogenase in streptozotocin-induced diabetic rat liver. |
| 373 | 17211564 | Glutathione-S-transferase (GST) catalyses the conjugation of glutathione with a variety of organic peroxides to form more water-soluble compounds. |
| 374 | 17211564 | Glucose-6-phosphate dehydrogenase (G6PDH) is essential to control intracellular reductive potential by increasing glutathione intracellular levels, which in turn decrease the amount of reactive oxygen species. |
| 375 | 17211564 | We investigated the activities of GST and G6PDH in the liver of both control and streptozotocin-induced diabetic rats. |
| 376 | 17211564 | Liver GST and G6PDH activities decreased significantly in five-week diabetic rats (p<0.001 and p<0.001 respectively) compared to controls and glyburide therapy restored these activities (p<0.001 for GST and p<0.001 for G6PDH). |
| 377 | 17211564 | The effect of the sulfonylurea glyburide on glutathione-S-transferase and glucose-6-phosphate dehydrogenase in streptozotocin-induced diabetic rat liver. |
| 378 | 17211564 | Glutathione-S-transferase (GST) catalyses the conjugation of glutathione with a variety of organic peroxides to form more water-soluble compounds. |
| 379 | 17211564 | Glucose-6-phosphate dehydrogenase (G6PDH) is essential to control intracellular reductive potential by increasing glutathione intracellular levels, which in turn decrease the amount of reactive oxygen species. |
| 380 | 17211564 | We investigated the activities of GST and G6PDH in the liver of both control and streptozotocin-induced diabetic rats. |
| 381 | 17211564 | Liver GST and G6PDH activities decreased significantly in five-week diabetic rats (p<0.001 and p<0.001 respectively) compared to controls and glyburide therapy restored these activities (p<0.001 for GST and p<0.001 for G6PDH). |
| 382 | 17338280 | Before treatment with NAC, glutathione peroxidase (GPx), catalase (CAT), and (GSH) levels of diabetic patients and control subjects showed no significant differences, whereas glutathione S-transferase (GST) levels were higher in type II diabetic patients. |
| 383 | 17338280 | Following 3 months of Following NAC supplementation, GSH, GST, and CAT levels were found to be similar to the levels before treatment. |
| 384 | 17338280 | Before treatment with NAC, glutathione peroxidase (GPx), catalase (CAT), and (GSH) levels of diabetic patients and control subjects showed no significant differences, whereas glutathione S-transferase (GST) levels were higher in type II diabetic patients. |
| 385 | 17338280 | Following 3 months of Following NAC supplementation, GSH, GST, and CAT levels were found to be similar to the levels before treatment. |
| 386 | 17496234 | The actions of a novel potent islet beta-cell specific ATP-sensitive K+ channel opener can be modulated by syntaxin-1A acting on sulfonylurea receptor 1. |
| 387 | 17496234 | We reported that syntaxin-1A binds nucleotide binding folds of sulfonylurea receptor 1 (SUR1) in beta-cells to inhibit K(ATP) channels. |
| 388 | 17496234 | Whole-cell and inside-out patch-clamp electrophysiology was used to examine the effects of glutathione S-transferase (GST)-syntaxin-1A dialysis or green fluorescence protein/syntaxin-1A cotransfection on NNC55-0462 actions. |
| 389 | 17496234 | Dialysis of GST-syntaxin-1A into the cell cytoplasm reduced both potency and efficacy of extracellularly perfused NNC55-0462 in a HEK cell line stably expressing Kir6.2/SUR1 (BA8 cells) and in rat islet beta-cells. |
| 390 | 17496234 | Moreover, inside-out membrane patches excised from BA8 cells showed that both GST-syntaxin-1A and its H3 domain inhibited K(ATP) channels previously activated by NNC55-0462. |
| 391 | 17496234 | This action on K(ATP) channels is isoform-specific to syntaxin-1A because syntaxin-2 was without effect. |
| 392 | 17496234 | Furthermore, the parent compound diazoxide showed similar sensitivity to GST-syntaxin-1A inhibition. |
| 393 | 17496234 | The actions of a novel potent islet beta-cell specific ATP-sensitive K+ channel opener can be modulated by syntaxin-1A acting on sulfonylurea receptor 1. |
| 394 | 17496234 | We reported that syntaxin-1A binds nucleotide binding folds of sulfonylurea receptor 1 (SUR1) in beta-cells to inhibit K(ATP) channels. |
| 395 | 17496234 | Whole-cell and inside-out patch-clamp electrophysiology was used to examine the effects of glutathione S-transferase (GST)-syntaxin-1A dialysis or green fluorescence protein/syntaxin-1A cotransfection on NNC55-0462 actions. |
| 396 | 17496234 | Dialysis of GST-syntaxin-1A into the cell cytoplasm reduced both potency and efficacy of extracellularly perfused NNC55-0462 in a HEK cell line stably expressing Kir6.2/SUR1 (BA8 cells) and in rat islet beta-cells. |
| 397 | 17496234 | Moreover, inside-out membrane patches excised from BA8 cells showed that both GST-syntaxin-1A and its H3 domain inhibited K(ATP) channels previously activated by NNC55-0462. |
| 398 | 17496234 | This action on K(ATP) channels is isoform-specific to syntaxin-1A because syntaxin-2 was without effect. |
| 399 | 17496234 | Furthermore, the parent compound diazoxide showed similar sensitivity to GST-syntaxin-1A inhibition. |
| 400 | 17496234 | The actions of a novel potent islet beta-cell specific ATP-sensitive K+ channel opener can be modulated by syntaxin-1A acting on sulfonylurea receptor 1. |
| 401 | 17496234 | We reported that syntaxin-1A binds nucleotide binding folds of sulfonylurea receptor 1 (SUR1) in beta-cells to inhibit K(ATP) channels. |
| 402 | 17496234 | Whole-cell and inside-out patch-clamp electrophysiology was used to examine the effects of glutathione S-transferase (GST)-syntaxin-1A dialysis or green fluorescence protein/syntaxin-1A cotransfection on NNC55-0462 actions. |
| 403 | 17496234 | Dialysis of GST-syntaxin-1A into the cell cytoplasm reduced both potency and efficacy of extracellularly perfused NNC55-0462 in a HEK cell line stably expressing Kir6.2/SUR1 (BA8 cells) and in rat islet beta-cells. |
| 404 | 17496234 | Moreover, inside-out membrane patches excised from BA8 cells showed that both GST-syntaxin-1A and its H3 domain inhibited K(ATP) channels previously activated by NNC55-0462. |
| 405 | 17496234 | This action on K(ATP) channels is isoform-specific to syntaxin-1A because syntaxin-2 was without effect. |
| 406 | 17496234 | Furthermore, the parent compound diazoxide showed similar sensitivity to GST-syntaxin-1A inhibition. |
| 407 | 17496234 | The actions of a novel potent islet beta-cell specific ATP-sensitive K+ channel opener can be modulated by syntaxin-1A acting on sulfonylurea receptor 1. |
| 408 | 17496234 | We reported that syntaxin-1A binds nucleotide binding folds of sulfonylurea receptor 1 (SUR1) in beta-cells to inhibit K(ATP) channels. |
| 409 | 17496234 | Whole-cell and inside-out patch-clamp electrophysiology was used to examine the effects of glutathione S-transferase (GST)-syntaxin-1A dialysis or green fluorescence protein/syntaxin-1A cotransfection on NNC55-0462 actions. |
| 410 | 17496234 | Dialysis of GST-syntaxin-1A into the cell cytoplasm reduced both potency and efficacy of extracellularly perfused NNC55-0462 in a HEK cell line stably expressing Kir6.2/SUR1 (BA8 cells) and in rat islet beta-cells. |
| 411 | 17496234 | Moreover, inside-out membrane patches excised from BA8 cells showed that both GST-syntaxin-1A and its H3 domain inhibited K(ATP) channels previously activated by NNC55-0462. |
| 412 | 17496234 | This action on K(ATP) channels is isoform-specific to syntaxin-1A because syntaxin-2 was without effect. |
| 413 | 17496234 | Furthermore, the parent compound diazoxide showed similar sensitivity to GST-syntaxin-1A inhibition. |
| 414 | 17537413 | The effect of EMS on glucose, insulin, hemoglobin, glycosylated hemoglobin, TBARS, hydroperoxide, superoxide dismutase (SOD), catalase (CAT), glutathione peroxide (Gpx), glutathione-S-transferase (GST), vitamins C and E, reduced glutathione (GSH) and membrane bound enzymes were studied. |
| 415 | 17537413 | The levels of glucose, glycosylated hemoglobin, TBARS, hyderoperoxide, and vitamin E were increased significantly whereas the level of insulin and hemoglobin, as well as antioxidants (SOD, CAT, Gpx, GST, vitamin C and GSH) membrane bound total ATPase, Na(+)/K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase were decreased significantly in streptozotocin-nicotinamide diabetic rats. |
| 416 | 17537413 | In addition the levels of insulin, hemoglobin, enzymic antioxidants, vitamin C, and GSH and the activities of membrane bound enzymes also were increased in EMS and metformin treated diabetic rats. |
| 417 | 17537413 | The effect of EMS on glucose, insulin, hemoglobin, glycosylated hemoglobin, TBARS, hydroperoxide, superoxide dismutase (SOD), catalase (CAT), glutathione peroxide (Gpx), glutathione-S-transferase (GST), vitamins C and E, reduced glutathione (GSH) and membrane bound enzymes were studied. |
| 418 | 17537413 | The levels of glucose, glycosylated hemoglobin, TBARS, hyderoperoxide, and vitamin E were increased significantly whereas the level of insulin and hemoglobin, as well as antioxidants (SOD, CAT, Gpx, GST, vitamin C and GSH) membrane bound total ATPase, Na(+)/K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase were decreased significantly in streptozotocin-nicotinamide diabetic rats. |
| 419 | 17537413 | In addition the levels of insulin, hemoglobin, enzymic antioxidants, vitamin C, and GSH and the activities of membrane bound enzymes also were increased in EMS and metformin treated diabetic rats. |
| 420 | 17570531 | These enzymes include aldehyde dehydrogenases (ALDH), aldo-keto reductases (AKR), carbonyl reductase (CBR), and glutathione S-transferases (GST). |
| 421 | 17573857 | Varying degree of reduction in the specific activities of antioxidant enzymes was evident in testis and ES, while the activity of glutathione-S-transferase (GST) was significantly elevated. |
| 422 | 17658503 | The liver and erythrocyte glutathione-S-transferase (GST) activity increased in all the groups treated with NDEA and PB. |
| 423 | 17693046 | The effect of THC and curcumin on glucose, insulin, haemoglobin, glycosylated haemoglobin, thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxide (Gpx), glutathione-S-transferase (GST), reduced glutathione (GSH) and membrane bound enzymes were studied. |
| 424 | 17693046 | The levels of blood glucose, glycosylated haemoglobin, erythrocyte TBARS, were increased significantly whereas the level of plasma insulin and haemoglobin, erythrocyte antioxidants (SOD, CAT, GPx, GST and GSH), membrane bound total ATPase, Na(+)/K(+)-ATPase, Ca(2+)-ATPase, Mg(2+)-ATPase were decreased significantly in diabetic rats. |
| 425 | 17693046 | The effect of THC and curcumin on glucose, insulin, haemoglobin, glycosylated haemoglobin, thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxide (Gpx), glutathione-S-transferase (GST), reduced glutathione (GSH) and membrane bound enzymes were studied. |
| 426 | 17693046 | The levels of blood glucose, glycosylated haemoglobin, erythrocyte TBARS, were increased significantly whereas the level of plasma insulin and haemoglobin, erythrocyte antioxidants (SOD, CAT, GPx, GST and GSH), membrane bound total ATPase, Na(+)/K(+)-ATPase, Ca(2+)-ATPase, Mg(2+)-ATPase were decreased significantly in diabetic rats. |
| 427 | 18311053 | Nuclear receptors have two regions for transactivation, a constitutive activation function (AF-1) and a ligand-dependent activation function (AF-2). |
| 428 | 18311053 | AF-1 and AF-2 seem to require interactions with coactivators for the activation function and both work synergistically to give full transactivation of nuclear receptors. |
| 429 | 18311053 | However, coactivators for AF-1 activity are poorly understood, whereas coactivators required for AF-2 activity have been well studied. |
| 430 | 18311053 | To understand the molecular mechanism of AF-1 in FXR, we isolated proteins associated with AF-1 by GST pull-down assay using the N-terminal region of FXR and nuclear extracts from HeLa cells. |
| 431 | 18370929 | To assess the contribution of individual tryptophan residues to this effect, we generated GST-GK [GK conjugated to GST (glutathione transferase)] and also pure GK with one, two or three of the tryptophan residues of GK replaced with other amino acids (i.e. |
| 432 | 18378083 | Furthermore, the activity of brain glutathione-S-transferase (GST) was significantly decreased and this was associated with a remarkable increase in brain lipid peroxidative parameter, thiobarbituric acid reactive substances (TBARS), as compared to sham control. |
| 433 | 18426076 | Glutathione S-transferase (GST) activity also was remarkably higher in STZ-induced diabetic rats than that in normal rats. |
| 434 | 18426076 | Insulin administered to STZ-induced diabetic rats prevented the hyperglycemia indicative of STZ-induced diabetes, but had no effect on the increased activities of GST. |
| 435 | 18426076 | On the other hand, the fluctuations in the enzymatic activities of FMO, UDP-glucuronosyltransferase, aryl sulphotransferase and glutathione related enzymes were restored to normal level by treatment with insulin in both diabetic rats. |
| 436 | 18426076 | Glutathione S-transferase (GST) activity also was remarkably higher in STZ-induced diabetic rats than that in normal rats. |
| 437 | 18426076 | Insulin administered to STZ-induced diabetic rats prevented the hyperglycemia indicative of STZ-induced diabetes, but had no effect on the increased activities of GST. |
| 438 | 18426076 | On the other hand, the fluctuations in the enzymatic activities of FMO, UDP-glucuronosyltransferase, aryl sulphotransferase and glutathione related enzymes were restored to normal level by treatment with insulin in both diabetic rats. |
| 439 | 19011089 | The adiponectin-interacting protein contains 2 thioredoxin domains and has very little sequence similarity to other GST isoforms. |
| 440 | 19011089 | DsbA-L expression in 3T3-L1 adipocytes is stimulated by the insulin sensitizer rosiglitazone and inhibited by the inflammatory cytokine TNFalpha. |
| 441 | 19011089 | Our results identify DsbA-L as a key regulator for adiponectin biosynthesis and uncover a potential new target for developing therapeutic drugs for the treatment of insulin resistance and its associated metabolic disorders. |
| 442 | 19130858 | Erythrocyte glutathione (GSH), superoxide dismutase (SOD) and thiobarbituric acid reactive substances (TBARS), plasma vitamins C and E and serum total glutathione-S-transferase (GST), protein thiols and ceruloplasmin (Cp) were estimated spectrophotometrically in maternal blood of age matched controls and mothers with GDM and also in cord blood samples of the above. |
| 443 | 19130858 | There was a significant increase in the erythrocytic GSH, serum total GST and protein thiols in GDM maternal blood when compared to controls whereas erythrocytic SOD exhibited a marked decrease in GDM cases. |
| 444 | 19130858 | Erythrocyte glutathione (GSH), superoxide dismutase (SOD) and thiobarbituric acid reactive substances (TBARS), plasma vitamins C and E and serum total glutathione-S-transferase (GST), protein thiols and ceruloplasmin (Cp) were estimated spectrophotometrically in maternal blood of age matched controls and mothers with GDM and also in cord blood samples of the above. |
| 445 | 19130858 | There was a significant increase in the erythrocytic GSH, serum total GST and protein thiols in GDM maternal blood when compared to controls whereas erythrocytic SOD exhibited a marked decrease in GDM cases. |
| 446 | 19406193 | The effect of bark extract on glucose, insulin, haemoglobin, glycosylated haemoglobin, TBARS, hydroperoxide, superoxide dismutase (SOD), catalase (CAT), glutathione peroxide (GPx), glutathione-S-transferase (GST), vitamins C and E, reduced glutathione (GSH) and membrane bound enzymes were studied. |
| 447 | 19487702 | Differential regulation of glycogenolysis by mutant protein phosphatase-1 glycogen-targeting subunits. |
| 448 | 19487702 | PTG and G(L) are hepatic protein phosphatase-1 (PP1) glycogen-targeting subunits, which direct PP1 activity against glycogen synthase (GS) and/or phosphorylase (GP). |
| 449 | 19487702 | As expected, GP binding to glutathione S-transferase (GST)-G(L)tr was reduced, whereas GP binding to GST-PTG-G(L) was increased 2- to 3-fold versus GST-PTG. |
| 450 | 19596526 | We analyzed the expression of glutathione S-transferases (GST) and cytochrome P450 enzymes (CYP) in 23 HCA, 20 HCC, and 22 focal nodular hyperplasias (FNH) using immunohistochemistry. |
| 451 | 19596526 | The liver tissue revealed consistent specific staining for GST alpha, CYP1A1, 1A2, 2E1, and 3A4. |
| 452 | 19596526 | Therefore, reduced expression of GST alpha and CYP3A4 may indicate specific metabolic defects in the tumor tissue characterizing subgroups of HCA and HCC. |
| 453 | 19596526 | We analyzed the expression of glutathione S-transferases (GST) and cytochrome P450 enzymes (CYP) in 23 HCA, 20 HCC, and 22 focal nodular hyperplasias (FNH) using immunohistochemistry. |
| 454 | 19596526 | The liver tissue revealed consistent specific staining for GST alpha, CYP1A1, 1A2, 2E1, and 3A4. |
| 455 | 19596526 | Therefore, reduced expression of GST alpha and CYP3A4 may indicate specific metabolic defects in the tumor tissue characterizing subgroups of HCA and HCC. |
| 456 | 19596526 | We analyzed the expression of glutathione S-transferases (GST) and cytochrome P450 enzymes (CYP) in 23 HCA, 20 HCC, and 22 focal nodular hyperplasias (FNH) using immunohistochemistry. |
| 457 | 19596526 | The liver tissue revealed consistent specific staining for GST alpha, CYP1A1, 1A2, 2E1, and 3A4. |
| 458 | 19596526 | Therefore, reduced expression of GST alpha and CYP3A4 may indicate specific metabolic defects in the tumor tissue characterizing subgroups of HCA and HCC. |
| 459 | 19616598 | The GLEt and glibenclamide were administered orally for 3 weeks and the effects on glucose, insulin, renal markers including urea, creatinine and uric acid, lipid peroxidation markers including thiobarbituric reactive substances (TBARS) and hydroperoxides and antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities in kidney were studied. |
| 460 | 19684436 | Oxidative stress was assessed by measuring cardiac and brain nitric oxide (NO), lipid peroxide levels, glutathione (GSH) and antioxidant enzyme activities, i.e. glutathione-S-transferase (GST) and catalase. |
| 461 | 19696094 | Herein, we tested the hypothesis that glutathione S-transferase P (GSTP), the GST isoform that displays high catalytic efficiency with acrolein, protects against CY-induced urotoxicity by detoxifying acrolein. |
| 462 | 19696094 | Treatment of wild-type (WT) and mGstP1/P2 null (GSTP-null) mice with CY caused hemorrhagic cystitis, edema, albumin extravasation, and sloughing of bladder epithelium; however, CY-induced bladder ulcerations of the lamina propria were more numerous and more severe in GSTP-null mice. |
| 463 | 19696094 | There was no difference in hepatic microsomal production of acrolein from CY or urinary hydroxypropyl mercapturic acid output between WT and GSTP-null mice, but CY induced greater c-Jun NH(2)-terminal kinase (JNK) and c-Jun, but not extracellular signal-regulated kinase or p38, activation in GSTP-null than in WT mice. |
| 464 | 20072924 | The observed elevated level of lipid peroxidation (LPO) comes down significantly (p < 0.05) and decreased activities of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) got increased (p < 0.05) significantly of diabetic rats on extract treatment. |
| 465 | 20186490 | After the treatment, the levels of urine sugar, blood glucose, liver glycogen, and antioxidants like vitamin C and E in plasma and superoxide dismutase (SOD), catalase (CAT), thiobarbituric acid reactive substances (TBARS), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) in liver, kidney and heart were determined. |
| 466 | 20186490 | Diabetic rats showed a significant (p < 0.05) elevation in glucose and TBARS and a significant (p < 0.05) reduction in glycogen, vitamin C and E, SOD, CAT, GPx, GST, and GSH levels when compared to normal control rats. |
| 467 | 20186490 | After the treatment, the levels of urine sugar, blood glucose, liver glycogen, and antioxidants like vitamin C and E in plasma and superoxide dismutase (SOD), catalase (CAT), thiobarbituric acid reactive substances (TBARS), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) in liver, kidney and heart were determined. |
| 468 | 20186490 | Diabetic rats showed a significant (p < 0.05) elevation in glucose and TBARS and a significant (p < 0.05) reduction in glycogen, vitamin C and E, SOD, CAT, GPx, GST, and GSH levels when compared to normal control rats. |
| 469 | 20307516 | After the experimental period of 30 days, the pathophysiological markers such as serum bilirubin and hepatic aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP) were studied in addition to hepatic TNF-alpha, IL-1 beta, IL-6, NF-kappaB p65 and nitric oxide (NO) levels in control and experimental groups of rats. |
| 470 | 20307516 | The levels of vitamin C, vitamin E and reduced glutathione (GSH) and activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST) and glutathione reductase (GR) were determined in the liver tissues. |
| 471 | 20333650 | Oral administration of resveratrol (5 mg/kg body weight) to diabetic rats for 30 days showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), TNF-alpha, IL-1beta, IL-6, NF-kappaB p65 unit and nitric oxide (NO) with concomitant elevation in plasma insulin. |
| 472 | 20333650 | The diminished activities of pancreatic superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione-S-transferase (GST) as well as the decreased levels of plasma ceruloplasmin, vitamin C, vitamin E and reduced glutathione (GSH) in diabetic rats were reverted to near normalcy by resveratrol administration. |
| 473 | 20398890 | Catalase (CAT) activity was significantly reduced while glutathione-S-transferase (GST) and glutathione reductase (GR) activities remained unchanged in the pancreas of diabetic rats. |
| 474 | 20422335 | The absence of cardiomyopathy is accompanied by increased activities of CAT, MnSOD and GST in long-term diabetes in rats. |
| 475 | 20422335 | The activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST), the incidence of DNA damage, the activation of poly (ADP-ribose) polymerase-1 (PARP-1), a marker of DNA repair, and connective tissue growth factor (CTGF), a marker of tissue fibrosis, were examined in the hearts of rats for 16 weeks after diabetes induction by streptozotocin (STZ) administration. |
| 476 | 20422335 | While total SOD and CuZn-SOD exhibited progressively decreasing activities, those of Mn-SOD and GST were elevated. |
| 477 | 20422335 | Neither DNA strand breaks (apoptosis or necrosis) nor changes in PARP-1 activity and in CTGF levels (fibrosis) were observed in the diabetic heart. |
| 478 | 20422335 | The absence of cardiomyopathy is accompanied with increased activities of CAT, MnSOD and GST. |
| 479 | 20422335 | The absence of cardiomyopathy is accompanied by increased activities of CAT, MnSOD and GST in long-term diabetes in rats. |
| 480 | 20422335 | The activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST), the incidence of DNA damage, the activation of poly (ADP-ribose) polymerase-1 (PARP-1), a marker of DNA repair, and connective tissue growth factor (CTGF), a marker of tissue fibrosis, were examined in the hearts of rats for 16 weeks after diabetes induction by streptozotocin (STZ) administration. |
| 481 | 20422335 | While total SOD and CuZn-SOD exhibited progressively decreasing activities, those of Mn-SOD and GST were elevated. |
| 482 | 20422335 | Neither DNA strand breaks (apoptosis or necrosis) nor changes in PARP-1 activity and in CTGF levels (fibrosis) were observed in the diabetic heart. |
| 483 | 20422335 | The absence of cardiomyopathy is accompanied with increased activities of CAT, MnSOD and GST. |
| 484 | 20422335 | The absence of cardiomyopathy is accompanied by increased activities of CAT, MnSOD and GST in long-term diabetes in rats. |
| 485 | 20422335 | The activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST), the incidence of DNA damage, the activation of poly (ADP-ribose) polymerase-1 (PARP-1), a marker of DNA repair, and connective tissue growth factor (CTGF), a marker of tissue fibrosis, were examined in the hearts of rats for 16 weeks after diabetes induction by streptozotocin (STZ) administration. |
| 486 | 20422335 | While total SOD and CuZn-SOD exhibited progressively decreasing activities, those of Mn-SOD and GST were elevated. |
| 487 | 20422335 | Neither DNA strand breaks (apoptosis or necrosis) nor changes in PARP-1 activity and in CTGF levels (fibrosis) were observed in the diabetic heart. |
| 488 | 20422335 | The absence of cardiomyopathy is accompanied with increased activities of CAT, MnSOD and GST. |
| 489 | 20422335 | The absence of cardiomyopathy is accompanied by increased activities of CAT, MnSOD and GST in long-term diabetes in rats. |
| 490 | 20422335 | The activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST), the incidence of DNA damage, the activation of poly (ADP-ribose) polymerase-1 (PARP-1), a marker of DNA repair, and connective tissue growth factor (CTGF), a marker of tissue fibrosis, were examined in the hearts of rats for 16 weeks after diabetes induction by streptozotocin (STZ) administration. |
| 491 | 20422335 | While total SOD and CuZn-SOD exhibited progressively decreasing activities, those of Mn-SOD and GST were elevated. |
| 492 | 20422335 | Neither DNA strand breaks (apoptosis or necrosis) nor changes in PARP-1 activity and in CTGF levels (fibrosis) were observed in the diabetic heart. |
| 493 | 20422335 | The absence of cardiomyopathy is accompanied with increased activities of CAT, MnSOD and GST. |
| 494 | 20521623 | Effect of GSTM1 and GSTT1 double deletions in the development of oxidative stress in diabetic nephropathy patients. |
| 495 | 20521623 | Association of diabetic nephropathy (DN) with the deletion of GSTT1 and GSTM1 genes is well reported. |
| 496 | 20521623 | Reduced-glutathione (GSH), glutathione S-transferase (GST) activity and malondialdehyde (MDA) levels were measured for the assessment of OS. |
| 497 | 20521623 | Genetic polymorphism analysis of DN patients revealed the following distribution pattern: GSTM1 null 46.7%; GSTT1 null 55%; both null 30% and both positive 28.3%. |
| 498 | 20521623 | Double deletions involving GSTT1 and GSTM1 may result in decreased GST levels, leading to increased OS as reflected by increased MDA levels. |
| 499 | 20521623 | Effect of GSTM1 and GSTT1 double deletions in the development of oxidative stress in diabetic nephropathy patients. |
| 500 | 20521623 | Association of diabetic nephropathy (DN) with the deletion of GSTT1 and GSTM1 genes is well reported. |
| 501 | 20521623 | Reduced-glutathione (GSH), glutathione S-transferase (GST) activity and malondialdehyde (MDA) levels were measured for the assessment of OS. |
| 502 | 20521623 | Genetic polymorphism analysis of DN patients revealed the following distribution pattern: GSTM1 null 46.7%; GSTT1 null 55%; both null 30% and both positive 28.3%. |
| 503 | 20521623 | Double deletions involving GSTT1 and GSTM1 may result in decreased GST levels, leading to increased OS as reflected by increased MDA levels. |
| 504 | 21170474 | Target DNA binding affinities have been quantified by electrophoretic mobility shift assay using bacterially expressed glutathione-S-transferase (GST)-HNF-1α fusion proteins and nuclear extracts of transfected Cos7 cells. |
| 505 | 21327985 | Control versus patient results in the univariate analysis were the following: pre-gestational body mass index [BMI] 23.31 ± 4.2 vs. 27.13 ± 4.6 kg/m(2) (P = 0.001); weeks at delivery 39.2 ± 3.05 vs. 38.9 ± 1.8 (P = 0.09); Caesarean delivery 12.5 vs. 43% (P = 0.004); macrosomia 4 vs. 9.4% (P = 0.6); lipoperoxides [LPO] 2.06 ± 1.00 vs. 3.14 ± 1.55 μmol/mg (P = 0.001); catalase 3.23 ± 1.41 vs. 2.52 ± 1.3 nmol/min/ml (P = 0.03); superoxide dismutase [SOD] 0.11 ± 0.04 vs. 0.08 ± 0.01 U/ml (P = 0.0003); glutathione peroxidase [GPX] 0.03 ± 0.006 vs. 0.025 ± 0.006 nmol/min/ml (P = 0.01); glutathione reductase [GSH] 0.004 ± 0.002 vs. 0.004 ± 0.004 nmol/min/ml (P = 0.9)]; and glutathione transferase [GST] 0.0025 ± 0.0012 vs. 0.0027 ± 0.00017 nmol/min/ml (P = 0.7). |
| 506 | 21382363 | The activities of antioxidant enzymes catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and the levels of low-molecular weight antioxidants Vitamin C, Vitamin E and reduced glutathione (GSH) were decreased while increases in the levels of lipid peroxidation markers were observed in liver and kidney tissues of diabetic control rats as compared to control rats. |
| 507 | 21479831 | Antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), as well as carbonic anhydrase (CA), myeloperoxidase (MPO) activities and protein carbonyl content (PCC) were determined in muscle tissue. |
| 508 | 22056647 | The activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and the levels of low-molecular weight antioxidants vitamin C, vitamin E and reduced glutathione (GSH) were decreased while increases in the levels of LPO markers were observed in liver and kidney tissues of diabetic control rats as compared to normal control rats. |
| 509 | 22058002 | Glutathione S-transferase (GST) protects cells against oxidative stress. |
| 510 | 22058002 | Two polymorphisms were identified by multiplex PCR within the GST genes: GSTM1 and GSTT1. |
| 511 | 22058002 | Glutathione S-transferase (GST) protects cells against oxidative stress. |
| 512 | 22058002 | Two polymorphisms were identified by multiplex PCR within the GST genes: GSTM1 and GSTT1. |
| 513 | 22086798 | Glutathione S-transferase (GST) M1 null genotype has been reported playing a significant role in the diabetes mellitus (DM) susceptibility in Turkish population. |
| 514 | 22086798 | We investigated whether the GSTM1, GSTA1, and GSTP1 gene polymorphisms are associated with posttransplantation diabetes mellitus (PTDM) in Taiwan. |
| 515 | 22086798 | The distributions of GSTA1, GSTP1, and GSTM1 genotypes alleles were not significantly different between PTDM and non-DM group. |
| 516 | 22086798 | Patients carrying the different GSTA1, GSTP1, and GSTM1 genetic and allelic polymorphisms had no differences for the development of PTDM. |
| 517 | 22086798 | These overall results suggested a lack of strong association with GSTA1, GSTP1, and GSTM1 genetic polymorphisms to the susceptibility of PTDM in Taiwanese RTRs. |
| 518 | 22086798 | Glutathione S-transferase (GST) M1 null genotype has been reported playing a significant role in the diabetes mellitus (DM) susceptibility in Turkish population. |
| 519 | 22086798 | We investigated whether the GSTM1, GSTA1, and GSTP1 gene polymorphisms are associated with posttransplantation diabetes mellitus (PTDM) in Taiwan. |
| 520 | 22086798 | The distributions of GSTA1, GSTP1, and GSTM1 genotypes alleles were not significantly different between PTDM and non-DM group. |
| 521 | 22086798 | Patients carrying the different GSTA1, GSTP1, and GSTM1 genetic and allelic polymorphisms had no differences for the development of PTDM. |
| 522 | 22086798 | These overall results suggested a lack of strong association with GSTA1, GSTP1, and GSTM1 genetic polymorphisms to the susceptibility of PTDM in Taiwanese RTRs. |
| 523 | 22086798 | Glutathione S-transferase (GST) M1 null genotype has been reported playing a significant role in the diabetes mellitus (DM) susceptibility in Turkish population. |
| 524 | 22086798 | We investigated whether the GSTM1, GSTA1, and GSTP1 gene polymorphisms are associated with posttransplantation diabetes mellitus (PTDM) in Taiwan. |
| 525 | 22086798 | The distributions of GSTA1, GSTP1, and GSTM1 genotypes alleles were not significantly different between PTDM and non-DM group. |
| 526 | 22086798 | Patients carrying the different GSTA1, GSTP1, and GSTM1 genetic and allelic polymorphisms had no differences for the development of PTDM. |
| 527 | 22086798 | These overall results suggested a lack of strong association with GSTA1, GSTP1, and GSTM1 genetic polymorphisms to the susceptibility of PTDM in Taiwanese RTRs. |
| 528 | 22086798 | Glutathione S-transferase (GST) M1 null genotype has been reported playing a significant role in the diabetes mellitus (DM) susceptibility in Turkish population. |
| 529 | 22086798 | We investigated whether the GSTM1, GSTA1, and GSTP1 gene polymorphisms are associated with posttransplantation diabetes mellitus (PTDM) in Taiwan. |
| 530 | 22086798 | The distributions of GSTA1, GSTP1, and GSTM1 genotypes alleles were not significantly different between PTDM and non-DM group. |
| 531 | 22086798 | Patients carrying the different GSTA1, GSTP1, and GSTM1 genetic and allelic polymorphisms had no differences for the development of PTDM. |
| 532 | 22086798 | These overall results suggested a lack of strong association with GSTA1, GSTP1, and GSTM1 genetic polymorphisms to the susceptibility of PTDM in Taiwanese RTRs. |
| 533 | 22086798 | Glutathione S-transferase (GST) M1 null genotype has been reported playing a significant role in the diabetes mellitus (DM) susceptibility in Turkish population. |
| 534 | 22086798 | We investigated whether the GSTM1, GSTA1, and GSTP1 gene polymorphisms are associated with posttransplantation diabetes mellitus (PTDM) in Taiwan. |
| 535 | 22086798 | The distributions of GSTA1, GSTP1, and GSTM1 genotypes alleles were not significantly different between PTDM and non-DM group. |
| 536 | 22086798 | Patients carrying the different GSTA1, GSTP1, and GSTM1 genetic and allelic polymorphisms had no differences for the development of PTDM. |
| 537 | 22086798 | These overall results suggested a lack of strong association with GSTA1, GSTP1, and GSTM1 genetic polymorphisms to the susceptibility of PTDM in Taiwanese RTRs. |
| 538 | 22573545 | The levels of superoxide dismutase and glutathione peroxidase did not change, but the levels of glutathione-S-transferase (GST) were increased in diabetic prostate. |
| 539 | 22652274 | The role of GSTM1, GSTT1, GSTP1, and OGG1 polymorphisms in type 2 diabetes mellitus risk: a case-control study in a Turkish population. |
| 540 | 22652274 | The aim of the present study was to investigate the role of some polymorphisms in GSTs (GSTM1, GSTT1 and GSTP1) which are very important protective mechanisms against oxidative stress and in OGG1 gene which is important in DNA repair, against the risk of type 2 diabetes mellitus (T2DM). 127 T2DM and 127 control subjects were included in the study. |
| 541 | 22652274 | Analyses of GSTM1 and GSTT1 gene polymorphisms were performed by allele specific PCR and those of GSTP1 Ile105Val and OGG1 Ser326Cys by PCR-RFLP. |
| 542 | 22652274 | Similarly, the risk of T2DM was statistically increased with GSTM1 null (OR=3.841, 95% CI=2.28-6.469), GSTT1 null+GSTP1 (H+M) (OR=4.118, 95% CI=1.327-12.778) and GSTM1 null+OGG1 (H+M) (OR=3.322, 95% CI=1.898-5.816) and GSTT1 null+OGG1 (H+M) (OR=2.179, 95% CI=1.083-4.386) as compared to the control group. |
| 543 | 22678714 | Glutathione peroxidase (GPx), glutathione transferase (GST), catalase (CAT) and NAD(P)H:quinine-oxidoreductase1 (NQO1) activity, and malondialdehyde (MDA) in the liver were evaluated. |
| 544 | 22678714 | GPx, GST and NQO1 activity were decreased in the liver, while MDA levels rose. |
| 545 | 22678714 | Glutathione peroxidase (GPx), glutathione transferase (GST), catalase (CAT) and NAD(P)H:quinine-oxidoreductase1 (NQO1) activity, and malondialdehyde (MDA) in the liver were evaluated. |
| 546 | 22678714 | GPx, GST and NQO1 activity were decreased in the liver, while MDA levels rose. |
| 547 | 22987311 | Cisplatin exposure induced oxidative stress as indicated by decreased levels of non-enzymatic antioxidant defenses [glutathione (GSH) and ascorbic acid levels] and components of the enzymatic antioxidant defenses [superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx), glutathione reductase (GR) and and glutathione S-transferase(GST) activities)] in renal tissue. |
| 548 | 22987311 | Pioglitazone protected against the inhibition of CAT, SOD, GPx, GR and GST activities induced by cisplatin in the kidneys of mice. |
| 549 | 22987311 | Cisplatin exposure induced oxidative stress as indicated by decreased levels of non-enzymatic antioxidant defenses [glutathione (GSH) and ascorbic acid levels] and components of the enzymatic antioxidant defenses [superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx), glutathione reductase (GR) and and glutathione S-transferase(GST) activities)] in renal tissue. |
| 550 | 22987311 | Pioglitazone protected against the inhibition of CAT, SOD, GPx, GR and GST activities induced by cisplatin in the kidneys of mice. |
| 551 | 23014993 | Study of the association between glutathione S-transferase (GSTM1, GSTT1, GSTP1) polymorphisms with type II diabetes mellitus in southern of Iran. |
| 552 | 23014993 | To investigate the association between GSTs polymorphism with type 2 diabetes mellitus (T2DM), we investigated the frequency of GSTM1, T1 and P1 genotypes in patients with T2DM and controls. |
| 553 | 23014993 | However, the frequency of GSTT1 (OR = 1.29; 95 % CI = 0.07-2.14, P = 0.367) and GSTP1 (OR = 0.83; 95 % CI = 0.53-1.30, P = 0.389) genotypes were not significantly different comparing both groups. |
| 554 | 23014993 | Our results indicated that GSTM1 and GSTT1 genotypes might be involved in the pathogenesis of T2DM in south Iranian population. |
| 555 | 23105641 | Biochemical parameters like plasma glucose, oral glucose tolerance and glycosylated hemoglobin HbA(1c), were measured along with lipid profile, and enzymes like glutathione peroxidase (GPX), lipid peroxidase (LPO), superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) in normal, untreated diabetic rats and diabetic rats treated withOcimum sanctum L extracts and vitamin E. |
| 556 | 23105641 | Evaluation of biochemical profile in treated groups showed statistically significant reduction in plasma levels of glucose, HbA(1c), lipid profile and LPO, and elevation of GPX, SOD, CAT and GST. |
| 557 | 23105641 | Biochemical parameters like plasma glucose, oral glucose tolerance and glycosylated hemoglobin HbA(1c), were measured along with lipid profile, and enzymes like glutathione peroxidase (GPX), lipid peroxidase (LPO), superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) in normal, untreated diabetic rats and diabetic rats treated withOcimum sanctum L extracts and vitamin E. |
| 558 | 23105641 | Evaluation of biochemical profile in treated groups showed statistically significant reduction in plasma levels of glucose, HbA(1c), lipid profile and LPO, and elevation of GPX, SOD, CAT and GST. |
| 559 | 23105888 | Copper and ceruloplasmin levels in relation to total thiols and GST in type 2 diabetes mellitus patients. |
| 560 | 23105888 | Current study was undertaken to know the relation between fasting plasma glucose (FPG) and copper along with antioxidants like total thiols and ceruloplasmin, and antioxidant enzyme glutathione S transferase (GST). |
| 561 | 23105888 | Plasma total thiols, GST, copper and ceruloplasmin levels were measured all the subjects using spectrophotometric methods and FPG levels were determined in clinical chemistry analyzer Hitachi 912. |
| 562 | 23105888 | Copper and ceruloplasmin levels in relation to total thiols and GST in type 2 diabetes mellitus patients. |
| 563 | 23105888 | Current study was undertaken to know the relation between fasting plasma glucose (FPG) and copper along with antioxidants like total thiols and ceruloplasmin, and antioxidant enzyme glutathione S transferase (GST). |
| 564 | 23105888 | Plasma total thiols, GST, copper and ceruloplasmin levels were measured all the subjects using spectrophotometric methods and FPG levels were determined in clinical chemistry analyzer Hitachi 912. |
| 565 | 23105888 | Copper and ceruloplasmin levels in relation to total thiols and GST in type 2 diabetes mellitus patients. |
| 566 | 23105888 | Current study was undertaken to know the relation between fasting plasma glucose (FPG) and copper along with antioxidants like total thiols and ceruloplasmin, and antioxidant enzyme glutathione S transferase (GST). |
| 567 | 23105888 | Plasma total thiols, GST, copper and ceruloplasmin levels were measured all the subjects using spectrophotometric methods and FPG levels were determined in clinical chemistry analyzer Hitachi 912. |
| 568 | 23111281 | Gene expression profiles of BB rat islets were highly distinct from F344 islets and under-expressed numerous genes involved in ROS metabolism, including glutathione S-transferase (GST) family members (Gstm2, Gstm4, Gstm7, Gstt1, Gstp1, and Gstk1), superoxide dismutases (Sod2 and Sod3), peroxidases, and peroxiredoxins. |
| 569 | 23285670 | Oxidative stress was measured by tissue LPO levels, reduced glutathione (GSH) contents and by enzymatic activities of glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT). |
| 570 | 23285670 | In addition, WS treated rats also showed a significant increase in the activities of antioxidant enzymes namely GPx, GR, GST, SOD and CAT when compared with type 2 diabetic control rats. |
| 571 | 23285670 | Oxidative stress was measured by tissue LPO levels, reduced glutathione (GSH) contents and by enzymatic activities of glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT). |
| 572 | 23285670 | In addition, WS treated rats also showed a significant increase in the activities of antioxidant enzymes namely GPx, GR, GST, SOD and CAT when compared with type 2 diabetic control rats. |
| 573 | 23292544 | In addition, decreased activities of hepatic antioxidant enzymes, i.e. glucose-6-phosphate dehydrogenase (G6PDH), glutathione peroxidase (GPx), glutathinone-S-tranferase (GST) and superoxide dismutase (SOD) were significantly increased by 34%, 61%, 19% and 53% respectively in mulberry leaves-treated diabetic rats as compared with diabetic control rats. |
| 574 | 23444338 | On the 60th day, skin tissue samples were taken, glutathione (GSH), lipid peroxidation (LPO), nonenzymatic glycosylation (NEG) and protein levels, catalase (CAT), superoxide dismutase (SOD) and glutathione-S-transferase (GST) activities were determined. |
| 575 | 23444338 | Blood glucose, skin LPO and NEG levels increased, but skin GSH levels and CAT, SOD and GST activities decreased in the STZ group. |
| 576 | 23444338 | On the 60th day, skin tissue samples were taken, glutathione (GSH), lipid peroxidation (LPO), nonenzymatic glycosylation (NEG) and protein levels, catalase (CAT), superoxide dismutase (SOD) and glutathione-S-transferase (GST) activities were determined. |
| 577 | 23444338 | Blood glucose, skin LPO and NEG levels increased, but skin GSH levels and CAT, SOD and GST activities decreased in the STZ group. |
| 578 | 23570881 | GSTM1, GSTT1, GSTP1, and GSTA1 genetic variants are not associated with coronary artery disease in Taiwan. |
| 579 | 23633864 | Livers were collected at the end of experiment for histopathology and estimation of reduced glutathione (GSH), thiobarbituric acid reacting substances (TBARS), protein carbonyls, glutathione S-transferase (GST), glucose-6-phosphate dehydrogenase (G6PD), Na(+)/K(+) ATPase and Mg(2)+ ATPase, cytochrome P450 (CYP) and glycogen. |
| 580 | 23633864 | There was an increase in the concentration of TBARS and protein carbonyls, and decrease in the concentration of GSH and glycogen, and the activity of GST, G6PD, Na(+)/K(+) ATPase and Mg(2)+ ATPase in diabetic livers, while treatment groups showed significant (P < 0.05) increase in the above parameters. |
| 581 | 23633864 | Livers were collected at the end of experiment for histopathology and estimation of reduced glutathione (GSH), thiobarbituric acid reacting substances (TBARS), protein carbonyls, glutathione S-transferase (GST), glucose-6-phosphate dehydrogenase (G6PD), Na(+)/K(+) ATPase and Mg(2)+ ATPase, cytochrome P450 (CYP) and glycogen. |
| 582 | 23633864 | There was an increase in the concentration of TBARS and protein carbonyls, and decrease in the concentration of GSH and glycogen, and the activity of GST, G6PD, Na(+)/K(+) ATPase and Mg(2)+ ATPase in diabetic livers, while treatment groups showed significant (P < 0.05) increase in the above parameters. |
| 583 | 23643483 | The GSTM1 null, GSTT1 null, GSTP1 A/B or B/B and GSTA1 A/B or B/B genotypes were determined and deemed to be high-risk genotypes. |
| 584 | 23643483 | Among never-smokers, carriers of one, and those of two or more high-risk GSTM1, GSTP1 or GSTA1 genotypes were at a higher risk for NAFLD than those who were not carriers [odds ratio (95% confidence interval): 2.6 (1.1-5.9) and 3.3 (1.3-8.1), respectively], and the risk was further increased among current-smokers [4.6 (1.6-13.0) and 5.4 (1.2-23.7), respectively]. |
| 585 | 23643483 | This is the first report to show that the combination of current-smoking and harboring high-risk GSTM1, GSTP1 and/or GSTA1 genotypes is interactively associated with the risk of NAFLD. |
| 586 | 23643483 | The GSTM1 null, GSTT1 null, GSTP1 A/B or B/B and GSTA1 A/B or B/B genotypes were determined and deemed to be high-risk genotypes. |
| 587 | 23643483 | Among never-smokers, carriers of one, and those of two or more high-risk GSTM1, GSTP1 or GSTA1 genotypes were at a higher risk for NAFLD than those who were not carriers [odds ratio (95% confidence interval): 2.6 (1.1-5.9) and 3.3 (1.3-8.1), respectively], and the risk was further increased among current-smokers [4.6 (1.6-13.0) and 5.4 (1.2-23.7), respectively]. |
| 588 | 23643483 | This is the first report to show that the combination of current-smoking and harboring high-risk GSTM1, GSTP1 and/or GSTA1 genotypes is interactively associated with the risk of NAFLD. |
| 589 | 23643483 | The GSTM1 null, GSTT1 null, GSTP1 A/B or B/B and GSTA1 A/B or B/B genotypes were determined and deemed to be high-risk genotypes. |
| 590 | 23643483 | Among never-smokers, carriers of one, and those of two or more high-risk GSTM1, GSTP1 or GSTA1 genotypes were at a higher risk for NAFLD than those who were not carriers [odds ratio (95% confidence interval): 2.6 (1.1-5.9) and 3.3 (1.3-8.1), respectively], and the risk was further increased among current-smokers [4.6 (1.6-13.0) and 5.4 (1.2-23.7), respectively]. |
| 591 | 23643483 | This is the first report to show that the combination of current-smoking and harboring high-risk GSTM1, GSTP1 and/or GSTA1 genotypes is interactively associated with the risk of NAFLD. |
| 592 | 23842942 | The anti obesity effect of water soluble fraction of Gymnema sylvestre extract (120 mg/kg, p.o. for 21 days) in HFD fed rats was evaluated by the measurement of body weight gain, food intake, hemodynamic changes (systolic, diastolic, mean blood pressure and heart rate), serum lipid profiles (triglycerides, total cholesterol, LDL-cholesterol, HDL-cholesterol), leptin, insulin, glucose, apolipoproteins A1 and B, lactate dehydrogenase (LDH) and antioxidant enzymes such as reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S transferase (GST), superoxide dismutase (SOD) and catalase (CAT) levels in liver tissues. |
| 593 | 23842942 | Water soluble fraction of G. sylvestre ethanolic extract and rimonabant significantly reduced serum lipids, leptin, insulin, glucose, apolipoprotein B and LDH levels while it significantly increased the HDL-cholesterol, apolipoprotein A1 and antioxidant enzymes levels in liver tissue as compared to the HFD fed rats. |
| 594 | 24008019 | To evaluate the association of GSTs (GSTM1, GSTT1 and GSTP1) gene polymorphisms with T2DM, a meta-analysis was performed before October, 2012. |
| 595 | 24008019 | There were a total of 1354/1666 (n=9) cases/controls (studies) for GSTM1, 1271/1470 (n=8) for GSTT1, and 1205/1250 (n=7) for GSTM1. |
| 596 | 24008019 | There were significant associations between GSTM1 polymorphism, GSTT1 polymorphism and T2DM in the contrast of present genotype vs. null genotype, with pooled OR=1.99 (95%CI=1.46-2.71) and OR=1.61 (95%CI=1.19-2.17), respectively. |
| 597 | 24008019 | When stratified by ethnicity, the significant associations were also existed in Asians for GSTM1 and GSTT1, but not GSTP1. |
| 598 | 24008019 | Finally, the accumulated evidence proved the obvious associations of GSTM1 and GSTT1 polymorphisms with an increased risk of T2DM. |