# |
PMID |
Sentence |
1 |
1720333
|
Coenzyme Q (CoQ0) and other quinones were shown to be potent insulin secretagogues in the isolated pancreatic islet.
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2 |
1720333
|
CoQ6 and CoQ10 (ubiquinone), duroquinone and durohydroquinone did not stimulate insulin release.
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3 |
7768357
|
The decrease in Eh7 of the mitochondrial NAD couple, Eh7NAD+/NADH, from -280 to -300 mV and the increase in Eh7 of the coenzyme Q couple, Eh7Q/QH2, from -4 to +12 mV was equivalent to an increase from -53 kJ to -60 kJ/2 mol e in the reaction catalyzed by the mitochondrial NADH dehydrogenase multienzyme complex (EC 1.6.5.3).
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4 |
10343974
|
Significant decrease was seen in activities of dinitrophenylhydrazine DNPH-coenzyme Q reductase (complex I), coenzyme Q cytochrome-c reductase (complex III), and cytochrome-c oxidase (complex IV) from discrete brain regions with more pronounced changes in complex I.
|
5 |
10343974
|
Succinate dehydrogenase (SDH) coenzyme Q reductase (complex II), which is an enzyme shared by tricarboxylic acid (TCA) cycle and electron transport chain, showed a significant increase under the same set of conditions.
|
6 |
10343974
|
Significant decrease was seen in activities of dinitrophenylhydrazine DNPH-coenzyme Q reductase (complex I), coenzyme Q cytochrome-c reductase (complex III), and cytochrome-c oxidase (complex IV) from discrete brain regions with more pronounced changes in complex I.
|
7 |
10343974
|
Succinate dehydrogenase (SDH) coenzyme Q reductase (complex II), which is an enzyme shared by tricarboxylic acid (TCA) cycle and electron transport chain, showed a significant increase under the same set of conditions.
|
8 |
10601810
|
Correction of pancreatic beta-cell dysfunction with coenzyme Q(10) in a patient with mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes syndrome and diabetes mellitus.
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9 |
10783493
|
It may now be feasible to target specific supplemental nutrients to each of the key dysfunctions which conspire to maintain hyperglycemia in type 2 diabetes: bioactive chromium for skeletal muscle insulin resistance, conjugated linoleic acid for adipocyte insulin resistance, high-dose biotin for excessive hepatic glucose output, and coenzyme Q(10) for beta cell failure.
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10 |
11095989
|
Mitochondrial function of complex I (NADH-coenzyme Q reductase) activity in cybrid cells between mitochondrial DNA (mtDNA)-deleted (rho(0)) HeLa cells and mtDNA from the proband was decreased by 35%.
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11 |
11502580
|
The susceptibility to oxidative stress and antioxidant capacity (in terms of glutathione, coenzyme Q, and vitamin E content) of testis mitochondrial preparations isolated from Goto-Kakizaki (GK) non-insulin-dependent diabetic rats and from Wistar control rats, 1 yr of age, was evaluated.
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12 |
11914748
|
Coenzyme Q(10) improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus.
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13 |
12242689
|
Effects of combined quercetin and coenzyme Q(10) treatment on oxidative stress in normal and diabetic rats.
|
14 |
12242689
|
Our objective was to determine if subacute treatment with combined antioxidants quercetin and coenzyme Q(10) (10 mg/kg/day ip for 14 days) affects the activities of antioxidant enzymes in normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats.
|
15 |
12242689
|
Quercetin treatment raised blood glucose concentrations in normal and diabetic rats, whereas treatment with coenzyme Q(10) did not.
|
16 |
12242689
|
Liver, kidney, heart, and brain tissues were excised and the activities of catalase, glutathione reductase, glutathione peroxidase, superoxide dismutase, and concentrations of oxidized and reduced glutathione were determined.
|
17 |
12242689
|
In heart, catalase activity was increased in diabetic animals and restored to normal levels after combined treatment with quercetin and coenzyme Q(10).
|
18 |
12242689
|
Cardiac superoxide dismutase was lower than normal in quercetin- and quercetin + coenzyme Q(10)-treated diabetic rats.
|
19 |
12242689
|
There were no adverse effects on oxidative stress markers after treatment with quercetin or coenzyme Q(10) singly or in combination.
|
20 |
12242689
|
In spite of the elevation of glucose, quercetin may be effective in reversing some effects of diabetes, but the combination of quercetin + coenzyme Q(10) did not increase effectiveness in reversing effects of diabetes.
|
21 |
12242689
|
Effects of combined quercetin and coenzyme Q(10) treatment on oxidative stress in normal and diabetic rats.
|
22 |
12242689
|
Our objective was to determine if subacute treatment with combined antioxidants quercetin and coenzyme Q(10) (10 mg/kg/day ip for 14 days) affects the activities of antioxidant enzymes in normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats.
|
23 |
12242689
|
Quercetin treatment raised blood glucose concentrations in normal and diabetic rats, whereas treatment with coenzyme Q(10) did not.
|
24 |
12242689
|
Liver, kidney, heart, and brain tissues were excised and the activities of catalase, glutathione reductase, glutathione peroxidase, superoxide dismutase, and concentrations of oxidized and reduced glutathione were determined.
|
25 |
12242689
|
In heart, catalase activity was increased in diabetic animals and restored to normal levels after combined treatment with quercetin and coenzyme Q(10).
|
26 |
12242689
|
Cardiac superoxide dismutase was lower than normal in quercetin- and quercetin + coenzyme Q(10)-treated diabetic rats.
|
27 |
12242689
|
There were no adverse effects on oxidative stress markers after treatment with quercetin or coenzyme Q(10) singly or in combination.
|
28 |
12242689
|
In spite of the elevation of glucose, quercetin may be effective in reversing some effects of diabetes, but the combination of quercetin + coenzyme Q(10) did not increase effectiveness in reversing effects of diabetes.
|
29 |
12242689
|
Effects of combined quercetin and coenzyme Q(10) treatment on oxidative stress in normal and diabetic rats.
|
30 |
12242689
|
Our objective was to determine if subacute treatment with combined antioxidants quercetin and coenzyme Q(10) (10 mg/kg/day ip for 14 days) affects the activities of antioxidant enzymes in normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats.
|
31 |
12242689
|
Quercetin treatment raised blood glucose concentrations in normal and diabetic rats, whereas treatment with coenzyme Q(10) did not.
|
32 |
12242689
|
Liver, kidney, heart, and brain tissues were excised and the activities of catalase, glutathione reductase, glutathione peroxidase, superoxide dismutase, and concentrations of oxidized and reduced glutathione were determined.
|
33 |
12242689
|
In heart, catalase activity was increased in diabetic animals and restored to normal levels after combined treatment with quercetin and coenzyme Q(10).
|
34 |
12242689
|
Cardiac superoxide dismutase was lower than normal in quercetin- and quercetin + coenzyme Q(10)-treated diabetic rats.
|
35 |
12242689
|
There were no adverse effects on oxidative stress markers after treatment with quercetin or coenzyme Q(10) singly or in combination.
|
36 |
12242689
|
In spite of the elevation of glucose, quercetin may be effective in reversing some effects of diabetes, but the combination of quercetin + coenzyme Q(10) did not increase effectiveness in reversing effects of diabetes.
|
37 |
12242689
|
Effects of combined quercetin and coenzyme Q(10) treatment on oxidative stress in normal and diabetic rats.
|
38 |
12242689
|
Our objective was to determine if subacute treatment with combined antioxidants quercetin and coenzyme Q(10) (10 mg/kg/day ip for 14 days) affects the activities of antioxidant enzymes in normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats.
|
39 |
12242689
|
Quercetin treatment raised blood glucose concentrations in normal and diabetic rats, whereas treatment with coenzyme Q(10) did not.
|
40 |
12242689
|
Liver, kidney, heart, and brain tissues were excised and the activities of catalase, glutathione reductase, glutathione peroxidase, superoxide dismutase, and concentrations of oxidized and reduced glutathione were determined.
|
41 |
12242689
|
In heart, catalase activity was increased in diabetic animals and restored to normal levels after combined treatment with quercetin and coenzyme Q(10).
|
42 |
12242689
|
Cardiac superoxide dismutase was lower than normal in quercetin- and quercetin + coenzyme Q(10)-treated diabetic rats.
|
43 |
12242689
|
There were no adverse effects on oxidative stress markers after treatment with quercetin or coenzyme Q(10) singly or in combination.
|
44 |
12242689
|
In spite of the elevation of glucose, quercetin may be effective in reversing some effects of diabetes, but the combination of quercetin + coenzyme Q(10) did not increase effectiveness in reversing effects of diabetes.
|
45 |
12242689
|
Effects of combined quercetin and coenzyme Q(10) treatment on oxidative stress in normal and diabetic rats.
|
46 |
12242689
|
Our objective was to determine if subacute treatment with combined antioxidants quercetin and coenzyme Q(10) (10 mg/kg/day ip for 14 days) affects the activities of antioxidant enzymes in normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats.
|
47 |
12242689
|
Quercetin treatment raised blood glucose concentrations in normal and diabetic rats, whereas treatment with coenzyme Q(10) did not.
|
48 |
12242689
|
Liver, kidney, heart, and brain tissues were excised and the activities of catalase, glutathione reductase, glutathione peroxidase, superoxide dismutase, and concentrations of oxidized and reduced glutathione were determined.
|
49 |
12242689
|
In heart, catalase activity was increased in diabetic animals and restored to normal levels after combined treatment with quercetin and coenzyme Q(10).
|
50 |
12242689
|
Cardiac superoxide dismutase was lower than normal in quercetin- and quercetin + coenzyme Q(10)-treated diabetic rats.
|
51 |
12242689
|
There were no adverse effects on oxidative stress markers after treatment with quercetin or coenzyme Q(10) singly or in combination.
|
52 |
12242689
|
In spite of the elevation of glucose, quercetin may be effective in reversing some effects of diabetes, but the combination of quercetin + coenzyme Q(10) did not increase effectiveness in reversing effects of diabetes.
|
53 |
12242689
|
Effects of combined quercetin and coenzyme Q(10) treatment on oxidative stress in normal and diabetic rats.
|
54 |
12242689
|
Our objective was to determine if subacute treatment with combined antioxidants quercetin and coenzyme Q(10) (10 mg/kg/day ip for 14 days) affects the activities of antioxidant enzymes in normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats.
|
55 |
12242689
|
Quercetin treatment raised blood glucose concentrations in normal and diabetic rats, whereas treatment with coenzyme Q(10) did not.
|
56 |
12242689
|
Liver, kidney, heart, and brain tissues were excised and the activities of catalase, glutathione reductase, glutathione peroxidase, superoxide dismutase, and concentrations of oxidized and reduced glutathione were determined.
|
57 |
12242689
|
In heart, catalase activity was increased in diabetic animals and restored to normal levels after combined treatment with quercetin and coenzyme Q(10).
|
58 |
12242689
|
Cardiac superoxide dismutase was lower than normal in quercetin- and quercetin + coenzyme Q(10)-treated diabetic rats.
|
59 |
12242689
|
There were no adverse effects on oxidative stress markers after treatment with quercetin or coenzyme Q(10) singly or in combination.
|
60 |
12242689
|
In spite of the elevation of glucose, quercetin may be effective in reversing some effects of diabetes, but the combination of quercetin + coenzyme Q(10) did not increase effectiveness in reversing effects of diabetes.
|
61 |
12242689
|
Effects of combined quercetin and coenzyme Q(10) treatment on oxidative stress in normal and diabetic rats.
|
62 |
12242689
|
Our objective was to determine if subacute treatment with combined antioxidants quercetin and coenzyme Q(10) (10 mg/kg/day ip for 14 days) affects the activities of antioxidant enzymes in normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats.
|
63 |
12242689
|
Quercetin treatment raised blood glucose concentrations in normal and diabetic rats, whereas treatment with coenzyme Q(10) did not.
|
64 |
12242689
|
Liver, kidney, heart, and brain tissues were excised and the activities of catalase, glutathione reductase, glutathione peroxidase, superoxide dismutase, and concentrations of oxidized and reduced glutathione were determined.
|
65 |
12242689
|
In heart, catalase activity was increased in diabetic animals and restored to normal levels after combined treatment with quercetin and coenzyme Q(10).
|
66 |
12242689
|
Cardiac superoxide dismutase was lower than normal in quercetin- and quercetin + coenzyme Q(10)-treated diabetic rats.
|
67 |
12242689
|
There were no adverse effects on oxidative stress markers after treatment with quercetin or coenzyme Q(10) singly or in combination.
|
68 |
12242689
|
In spite of the elevation of glucose, quercetin may be effective in reversing some effects of diabetes, but the combination of quercetin + coenzyme Q(10) did not increase effectiveness in reversing effects of diabetes.
|
69 |
12732401
|
We therefore aimed to assess the independent and combined effects of fenofibrate and coenzyme Q(10) (CoQ) on endothelium-dependent and endothelium-independent vasodilator function of the forearm microcirculation in type 2 diabetes.
|
70 |
12861406
|
Insulin-like growth factor I (IGF-1) supplementation prevents diabetes-induced alterations in coenzymes Q9 and Q10.
|
71 |
12861406
|
Insulin-like growth factor 1 (IGF-1) is considered to be an "essential surviving factor", the level and function of which are compromised in diabetes.
|
72 |
12861406
|
Coenzyme Q(9) and Q(10) levels were assessed by ultraviolet detection on high pressure liquid chromatography.
|
73 |
12861406
|
IGF-1 supplementation prevented liver alterations in Q(10) but not Q(9) levels.
|
74 |
12861406
|
Q(9) and Q(10) levels in diabetic kidney were significantly depressed, and these deleterious effects were abolished by IGF-1 treatment.
|
75 |
12861406
|
These data suggest that IGF-1 antagonizes the diabetes-induced alterations in endogenous antioxidants including coenzyme Q(10), and hence may have a therapeutic role in diabetes.
|
76 |
12861406
|
Insulin-like growth factor I (IGF-1) supplementation prevents diabetes-induced alterations in coenzymes Q9 and Q10.
|
77 |
12861406
|
Insulin-like growth factor 1 (IGF-1) is considered to be an "essential surviving factor", the level and function of which are compromised in diabetes.
|
78 |
12861406
|
Coenzyme Q(9) and Q(10) levels were assessed by ultraviolet detection on high pressure liquid chromatography.
|
79 |
12861406
|
IGF-1 supplementation prevented liver alterations in Q(10) but not Q(9) levels.
|
80 |
12861406
|
Q(9) and Q(10) levels in diabetic kidney were significantly depressed, and these deleterious effects were abolished by IGF-1 treatment.
|
81 |
12861406
|
These data suggest that IGF-1 antagonizes the diabetes-induced alterations in endogenous antioxidants including coenzyme Q(10), and hence may have a therapeutic role in diabetes.
|
82 |
15075342
|
Coenzyme Q(0) (Q(0)), a strong electrophile, is toxic to insulin-producing cells.
|
83 |
15075342
|
Western analysis also showed that Q bonds to the E2 components of the purified KDC and (0)the pyruvate dehydrogenase complex (PDC).
|
84 |
15721028
|
Endothelium-ameliorating effects of statin therapy and coenzyme Q10 reductions in chronic heart failure.
|
85 |
15721028
|
However, statin therapy reduces plasma levels of coenzyme Q(10) (ubiquinone), which may have adverse effects on heart failure states.
|
86 |
15721028
|
Furthermore, we assessed how reductions in coenzyme Q(10) levels impact on potentially improved endothelial function.
|
87 |
15721028
|
Atorvastatin treatment lowered triglycerides, LDL-cholesterol and coenzyme Q(10) levels (all p<0.001) and improved endothelium-dependent vasodilatation during acetylcholine infusion (p=0.015).
|
88 |
15721028
|
Endothelium-dependent forearm blood flow improvements correlated with reductions in coenzyme Q(10) levels (p=0.011), but not with LDL-cholesterol levels (p=0.084).
|
89 |
15721028
|
Coenzyme Q(10) remained the significant variable predicting improvement in NO dependent endothelial function after adjusting for LDL-cholesterol levels (p=0.041).
|
90 |
15721028
|
Further studies are required to determine whether coenzyme Q(10) reductions are limiting the maximum favourable effects of statin therapy on the microcirculation.
|
91 |
15721028
|
Endothelium-ameliorating effects of statin therapy and coenzyme Q10 reductions in chronic heart failure.
|
92 |
15721028
|
However, statin therapy reduces plasma levels of coenzyme Q(10) (ubiquinone), which may have adverse effects on heart failure states.
|
93 |
15721028
|
Furthermore, we assessed how reductions in coenzyme Q(10) levels impact on potentially improved endothelial function.
|
94 |
15721028
|
Atorvastatin treatment lowered triglycerides, LDL-cholesterol and coenzyme Q(10) levels (all p<0.001) and improved endothelium-dependent vasodilatation during acetylcholine infusion (p=0.015).
|
95 |
15721028
|
Endothelium-dependent forearm blood flow improvements correlated with reductions in coenzyme Q(10) levels (p=0.011), but not with LDL-cholesterol levels (p=0.084).
|
96 |
15721028
|
Coenzyme Q(10) remained the significant variable predicting improvement in NO dependent endothelial function after adjusting for LDL-cholesterol levels (p=0.041).
|
97 |
15721028
|
Further studies are required to determine whether coenzyme Q(10) reductions are limiting the maximum favourable effects of statin therapy on the microcirculation.
|
98 |
15721028
|
Endothelium-ameliorating effects of statin therapy and coenzyme Q10 reductions in chronic heart failure.
|
99 |
15721028
|
However, statin therapy reduces plasma levels of coenzyme Q(10) (ubiquinone), which may have adverse effects on heart failure states.
|
100 |
15721028
|
Furthermore, we assessed how reductions in coenzyme Q(10) levels impact on potentially improved endothelial function.
|
101 |
15721028
|
Atorvastatin treatment lowered triglycerides, LDL-cholesterol and coenzyme Q(10) levels (all p<0.001) and improved endothelium-dependent vasodilatation during acetylcholine infusion (p=0.015).
|
102 |
15721028
|
Endothelium-dependent forearm blood flow improvements correlated with reductions in coenzyme Q(10) levels (p=0.011), but not with LDL-cholesterol levels (p=0.084).
|
103 |
15721028
|
Coenzyme Q(10) remained the significant variable predicting improvement in NO dependent endothelial function after adjusting for LDL-cholesterol levels (p=0.041).
|
104 |
15721028
|
Further studies are required to determine whether coenzyme Q(10) reductions are limiting the maximum favourable effects of statin therapy on the microcirculation.
|
105 |
15721028
|
Endothelium-ameliorating effects of statin therapy and coenzyme Q10 reductions in chronic heart failure.
|
106 |
15721028
|
However, statin therapy reduces plasma levels of coenzyme Q(10) (ubiquinone), which may have adverse effects on heart failure states.
|
107 |
15721028
|
Furthermore, we assessed how reductions in coenzyme Q(10) levels impact on potentially improved endothelial function.
|
108 |
15721028
|
Atorvastatin treatment lowered triglycerides, LDL-cholesterol and coenzyme Q(10) levels (all p<0.001) and improved endothelium-dependent vasodilatation during acetylcholine infusion (p=0.015).
|
109 |
15721028
|
Endothelium-dependent forearm blood flow improvements correlated with reductions in coenzyme Q(10) levels (p=0.011), but not with LDL-cholesterol levels (p=0.084).
|
110 |
15721028
|
Coenzyme Q(10) remained the significant variable predicting improvement in NO dependent endothelial function after adjusting for LDL-cholesterol levels (p=0.041).
|
111 |
15721028
|
Further studies are required to determine whether coenzyme Q(10) reductions are limiting the maximum favourable effects of statin therapy on the microcirculation.
|
112 |
15721028
|
Endothelium-ameliorating effects of statin therapy and coenzyme Q10 reductions in chronic heart failure.
|
113 |
15721028
|
However, statin therapy reduces plasma levels of coenzyme Q(10) (ubiquinone), which may have adverse effects on heart failure states.
|
114 |
15721028
|
Furthermore, we assessed how reductions in coenzyme Q(10) levels impact on potentially improved endothelial function.
|
115 |
15721028
|
Atorvastatin treatment lowered triglycerides, LDL-cholesterol and coenzyme Q(10) levels (all p<0.001) and improved endothelium-dependent vasodilatation during acetylcholine infusion (p=0.015).
|
116 |
15721028
|
Endothelium-dependent forearm blood flow improvements correlated with reductions in coenzyme Q(10) levels (p=0.011), but not with LDL-cholesterol levels (p=0.084).
|
117 |
15721028
|
Coenzyme Q(10) remained the significant variable predicting improvement in NO dependent endothelial function after adjusting for LDL-cholesterol levels (p=0.041).
|
118 |
15721028
|
Further studies are required to determine whether coenzyme Q(10) reductions are limiting the maximum favourable effects of statin therapy on the microcirculation.
|
119 |
15721028
|
Endothelium-ameliorating effects of statin therapy and coenzyme Q10 reductions in chronic heart failure.
|
120 |
15721028
|
However, statin therapy reduces plasma levels of coenzyme Q(10) (ubiquinone), which may have adverse effects on heart failure states.
|
121 |
15721028
|
Furthermore, we assessed how reductions in coenzyme Q(10) levels impact on potentially improved endothelial function.
|
122 |
15721028
|
Atorvastatin treatment lowered triglycerides, LDL-cholesterol and coenzyme Q(10) levels (all p<0.001) and improved endothelium-dependent vasodilatation during acetylcholine infusion (p=0.015).
|
123 |
15721028
|
Endothelium-dependent forearm blood flow improvements correlated with reductions in coenzyme Q(10) levels (p=0.011), but not with LDL-cholesterol levels (p=0.084).
|
124 |
15721028
|
Coenzyme Q(10) remained the significant variable predicting improvement in NO dependent endothelial function after adjusting for LDL-cholesterol levels (p=0.041).
|
125 |
15721028
|
Further studies are required to determine whether coenzyme Q(10) reductions are limiting the maximum favourable effects of statin therapy on the microcirculation.
|
126 |
15754849
|
Lp(a), triglycerides, blood glucose, plasma insulin, malondialdehyde, diene conjugates, TBARS and TNF-alpha and IL-6 levels, which were significantly greater during the acute phase, showed a significant decline and serum nitrite and coenzyme Q demonstrated an increase at 4 weeks of follow-up when the acute reactions evoked by MI had been controlled.
|
127 |
16375724
|
The emerging role of coenzyme Q-10 in aging, neurodegeneration, cardiovascular disease, cancer and diabetes mellitus.
|
128 |
16375724
|
Coenzyme Q-10 functions as a lipid antioxidant regulating membrane fluidity, recycling radical forms of vitamin C and E, and protecting membrane phospholipids against peroxidation.
|
129 |
16375724
|
Coenzyme Q-10 is a ubiquitous and endogenous lipid-soluble antioxidant found in all organisms.
|
130 |
16375724
|
The emerging role of coenzyme Q-10 in aging, neurodegeneration, cardiovascular disease, cancer and diabetes mellitus.
|
131 |
16375724
|
Coenzyme Q-10 functions as a lipid antioxidant regulating membrane fluidity, recycling radical forms of vitamin C and E, and protecting membrane phospholipids against peroxidation.
|
132 |
16375724
|
Coenzyme Q-10 is a ubiquitous and endogenous lipid-soluble antioxidant found in all organisms.
|
133 |
16375724
|
The emerging role of coenzyme Q-10 in aging, neurodegeneration, cardiovascular disease, cancer and diabetes mellitus.
|
134 |
16375724
|
Coenzyme Q-10 functions as a lipid antioxidant regulating membrane fluidity, recycling radical forms of vitamin C and E, and protecting membrane phospholipids against peroxidation.
|
135 |
16375724
|
Coenzyme Q-10 is a ubiquitous and endogenous lipid-soluble antioxidant found in all organisms.
|
136 |
16948477
|
Several mitochondrial parameters were evaluated: respiratory indexes (state 3 and 4 of respiration, respiratory control and ADP/O ratios), transmembrane potential, depolarization and repolarization levels, ATP, glutathione and coenzyme Q contents, production of hydrogen peroxide, superoxide dismutase, glutathione peroxidase and glutathione reductase activities and the ability of mitochondria to accumulate calcium.
|
137 |
17059463
|
Inhibition of the mitochondrial adenine nucleotide translocator (ANT) by long-chain acyl-CoA esters has been proposed to contribute to cellular dysfunction in obesity and type 2 diabetes by increasing formation of reactive oxygen species and adenosine via effects on the coenzyme Q redox state, mitochondrial membrane potential (Deltapsi) and cytosolic ATP concentrations.
|
138 |
17116186
|
Oxidative burden in prediabetic and diabetic individuals: evidence from plasma coenzyme Q(10).
|
139 |
17950797
|
Effect of coenzyme Q(10) supplementation on simvastatin-induced myalgia.
|
140 |
17950797
|
One postulated mechanism for statin-related myalgia is mitochondrial dysfunction through the depletion of coenzyme Q(10), a key component of the mitochondrial electron transport chain.
|
141 |
17950797
|
This pilot study evaluated the effect of coenzyme Q(10) supplementation on statin tolerance and myalgia in patients with previous statin-related myalgia.
|
142 |
17950797
|
Forty-four patients were randomized to coenzyme Q(10) (200 mg/day) or placebo for 12 weeks in combination with upward dose titration of simvastatin from 10 mg/day, doubling every 4 weeks if tolerated to a maximum of 40 mg/day.
|
143 |
17950797
|
There was no difference between combined therapy and statin alone in the myalgia score change (median 6.0 [interquartile range 2.1 to 8.8] vs 2.3 [0 to 12.8], p = 0.63), in the number of patients tolerating simvastatin 40 mg/day (16 of 22 [73%] with coenzyme Q(10) vs 13 of 22 [59%] with placebo, p = 0.34), or in the number of patients remaining on therapy (16 of 22 [73%] with coenzyme Q(10) vs 18 of 22 [82%] with placebo, p = 0.47).
|
144 |
17950797
|
In conclusion, coenzyme Q(10) supplementation did not improve statin tolerance or myalgia, although further studies are warranted.
|
145 |
17950797
|
Effect of coenzyme Q(10) supplementation on simvastatin-induced myalgia.
|
146 |
17950797
|
One postulated mechanism for statin-related myalgia is mitochondrial dysfunction through the depletion of coenzyme Q(10), a key component of the mitochondrial electron transport chain.
|
147 |
17950797
|
This pilot study evaluated the effect of coenzyme Q(10) supplementation on statin tolerance and myalgia in patients with previous statin-related myalgia.
|
148 |
17950797
|
Forty-four patients were randomized to coenzyme Q(10) (200 mg/day) or placebo for 12 weeks in combination with upward dose titration of simvastatin from 10 mg/day, doubling every 4 weeks if tolerated to a maximum of 40 mg/day.
|
149 |
17950797
|
There was no difference between combined therapy and statin alone in the myalgia score change (median 6.0 [interquartile range 2.1 to 8.8] vs 2.3 [0 to 12.8], p = 0.63), in the number of patients tolerating simvastatin 40 mg/day (16 of 22 [73%] with coenzyme Q(10) vs 13 of 22 [59%] with placebo, p = 0.34), or in the number of patients remaining on therapy (16 of 22 [73%] with coenzyme Q(10) vs 18 of 22 [82%] with placebo, p = 0.47).
|
150 |
17950797
|
In conclusion, coenzyme Q(10) supplementation did not improve statin tolerance or myalgia, although further studies are warranted.
|
151 |
17950797
|
Effect of coenzyme Q(10) supplementation on simvastatin-induced myalgia.
|
152 |
17950797
|
One postulated mechanism for statin-related myalgia is mitochondrial dysfunction through the depletion of coenzyme Q(10), a key component of the mitochondrial electron transport chain.
|
153 |
17950797
|
This pilot study evaluated the effect of coenzyme Q(10) supplementation on statin tolerance and myalgia in patients with previous statin-related myalgia.
|
154 |
17950797
|
Forty-four patients were randomized to coenzyme Q(10) (200 mg/day) or placebo for 12 weeks in combination with upward dose titration of simvastatin from 10 mg/day, doubling every 4 weeks if tolerated to a maximum of 40 mg/day.
|
155 |
17950797
|
There was no difference between combined therapy and statin alone in the myalgia score change (median 6.0 [interquartile range 2.1 to 8.8] vs 2.3 [0 to 12.8], p = 0.63), in the number of patients tolerating simvastatin 40 mg/day (16 of 22 [73%] with coenzyme Q(10) vs 13 of 22 [59%] with placebo, p = 0.34), or in the number of patients remaining on therapy (16 of 22 [73%] with coenzyme Q(10) vs 18 of 22 [82%] with placebo, p = 0.47).
|
156 |
17950797
|
In conclusion, coenzyme Q(10) supplementation did not improve statin tolerance or myalgia, although further studies are warranted.
|
157 |
17950797
|
Effect of coenzyme Q(10) supplementation on simvastatin-induced myalgia.
|
158 |
17950797
|
One postulated mechanism for statin-related myalgia is mitochondrial dysfunction through the depletion of coenzyme Q(10), a key component of the mitochondrial electron transport chain.
|
159 |
17950797
|
This pilot study evaluated the effect of coenzyme Q(10) supplementation on statin tolerance and myalgia in patients with previous statin-related myalgia.
|
160 |
17950797
|
Forty-four patients were randomized to coenzyme Q(10) (200 mg/day) or placebo for 12 weeks in combination with upward dose titration of simvastatin from 10 mg/day, doubling every 4 weeks if tolerated to a maximum of 40 mg/day.
|
161 |
17950797
|
There was no difference between combined therapy and statin alone in the myalgia score change (median 6.0 [interquartile range 2.1 to 8.8] vs 2.3 [0 to 12.8], p = 0.63), in the number of patients tolerating simvastatin 40 mg/day (16 of 22 [73%] with coenzyme Q(10) vs 13 of 22 [59%] with placebo, p = 0.34), or in the number of patients remaining on therapy (16 of 22 [73%] with coenzyme Q(10) vs 18 of 22 [82%] with placebo, p = 0.47).
|
162 |
17950797
|
In conclusion, coenzyme Q(10) supplementation did not improve statin tolerance or myalgia, although further studies are warranted.
|
163 |
17950797
|
Effect of coenzyme Q(10) supplementation on simvastatin-induced myalgia.
|
164 |
17950797
|
One postulated mechanism for statin-related myalgia is mitochondrial dysfunction through the depletion of coenzyme Q(10), a key component of the mitochondrial electron transport chain.
|
165 |
17950797
|
This pilot study evaluated the effect of coenzyme Q(10) supplementation on statin tolerance and myalgia in patients with previous statin-related myalgia.
|
166 |
17950797
|
Forty-four patients were randomized to coenzyme Q(10) (200 mg/day) or placebo for 12 weeks in combination with upward dose titration of simvastatin from 10 mg/day, doubling every 4 weeks if tolerated to a maximum of 40 mg/day.
|
167 |
17950797
|
There was no difference between combined therapy and statin alone in the myalgia score change (median 6.0 [interquartile range 2.1 to 8.8] vs 2.3 [0 to 12.8], p = 0.63), in the number of patients tolerating simvastatin 40 mg/day (16 of 22 [73%] with coenzyme Q(10) vs 13 of 22 [59%] with placebo, p = 0.34), or in the number of patients remaining on therapy (16 of 22 [73%] with coenzyme Q(10) vs 18 of 22 [82%] with placebo, p = 0.47).
|
168 |
17950797
|
In conclusion, coenzyme Q(10) supplementation did not improve statin tolerance or myalgia, although further studies are warranted.
|
169 |
17950797
|
Effect of coenzyme Q(10) supplementation on simvastatin-induced myalgia.
|
170 |
17950797
|
One postulated mechanism for statin-related myalgia is mitochondrial dysfunction through the depletion of coenzyme Q(10), a key component of the mitochondrial electron transport chain.
|
171 |
17950797
|
This pilot study evaluated the effect of coenzyme Q(10) supplementation on statin tolerance and myalgia in patients with previous statin-related myalgia.
|
172 |
17950797
|
Forty-four patients were randomized to coenzyme Q(10) (200 mg/day) or placebo for 12 weeks in combination with upward dose titration of simvastatin from 10 mg/day, doubling every 4 weeks if tolerated to a maximum of 40 mg/day.
|
173 |
17950797
|
There was no difference between combined therapy and statin alone in the myalgia score change (median 6.0 [interquartile range 2.1 to 8.8] vs 2.3 [0 to 12.8], p = 0.63), in the number of patients tolerating simvastatin 40 mg/day (16 of 22 [73%] with coenzyme Q(10) vs 13 of 22 [59%] with placebo, p = 0.34), or in the number of patients remaining on therapy (16 of 22 [73%] with coenzyme Q(10) vs 18 of 22 [82%] with placebo, p = 0.47).
|
174 |
17950797
|
In conclusion, coenzyme Q(10) supplementation did not improve statin tolerance or myalgia, although further studies are warranted.
|
175 |
18805359
|
In the majority of cases, dysfunction of the respiratory chain (particularly complexes I, II, IV, or V), of coenzyme Q, or of the pyruvate dehydrogenase complex are responsible for the disease.
|
176 |
18806896
|
Coenzyme Q(10) and alpha-lipoic acid supplementation in diabetic rats: conduction velocity distributions.
|
177 |
18806896
|
This study aims to investigate diabetes- and coenzyme Q(10) (CoQ(10)) or alpha-lipoic acid (ALA) supplementation-induced changes in the conduction velocity (CV) distributions of rat sciatic nerve fibers.
|
178 |
18806896
|
Coenzyme Q(10) (CoQ(10)) supplementation was found to have some positive effect on the diabetes-induced alterations.
|
179 |
18806896
|
Coenzyme Q(10) and alpha-lipoic acid supplementation in diabetic rats: conduction velocity distributions.
|
180 |
18806896
|
This study aims to investigate diabetes- and coenzyme Q(10) (CoQ(10)) or alpha-lipoic acid (ALA) supplementation-induced changes in the conduction velocity (CV) distributions of rat sciatic nerve fibers.
|
181 |
18806896
|
Coenzyme Q(10) (CoQ(10)) supplementation was found to have some positive effect on the diabetes-induced alterations.
|
182 |
18806896
|
Coenzyme Q(10) and alpha-lipoic acid supplementation in diabetic rats: conduction velocity distributions.
|
183 |
18806896
|
This study aims to investigate diabetes- and coenzyme Q(10) (CoQ(10)) or alpha-lipoic acid (ALA) supplementation-induced changes in the conduction velocity (CV) distributions of rat sciatic nerve fibers.
|
184 |
18806896
|
Coenzyme Q(10) (CoQ(10)) supplementation was found to have some positive effect on the diabetes-induced alterations.
|
185 |
19202203
|
Administration of simvastatin (10 mg/kg) to the diabetic-hypercholesterolaemic rats counteracted increased myocardial (coenzyme Q10, p < 0.05) and liver (total coenzyme Q9, p < 0.05) coenzyme Q concentrations but did not improve alpha-tocopherol depletion and increased formation of TBARS in the liver.
|
186 |
21674640
|
Coenzyme Q(10) , endothelial function, and cardiovascular disease.
|
187 |
21674640
|
Since the time a precise role of coenzyme Q(10) (CoQ(10) ) in myocardial bioenergetics was established, the involvement of CoQ in the pathophysiology of heart failure was hypothesized.
|
188 |
21674640
|
Coenzyme Q(10) , endothelial function, and cardiovascular disease.
|
189 |
21674640
|
Since the time a precise role of coenzyme Q(10) (CoQ(10) ) in myocardial bioenergetics was established, the involvement of CoQ in the pathophysiology of heart failure was hypothesized.
|
190 |
21940403
|
Mitochondrial superoxide and coenzyme Q in insulin-deficient rats: increased electron leak.
|
191 |
22226887
|
Observed defects include an impaired reduced glutathione metabolism and lowered intake and absorption of fat-soluble antioxidants (vitamin E, carotenoids, coenzyme Q-10, some polyunsaturated fatty acids, etc.) and oligoelements (such as Se, Cu and Zn) that are involved in reactive oxygen species detoxification by means of enzymatic defenses.
|
192 |
22328876
|
Reduced coenzyme Q(10) in female smokers and its association with lipid profile in a young healthy adult population.
|
193 |
22586586
|
Mitochondrial fatty acid oxidation is the source of the increased net ROS production, and the site of electron leakage is located proximal to coenzyme Q at the electron transfer flavoprotein that shuttles electrons from acyl-CoA dehydrogenases to coenzyme Q.
|
194 |
23265517
|
After 12 weeks, RBBO significantly decreased malondialdehyde and restored superoxide dismutase, catalase, glutathione peroxidase, coenzyme Q(10) and ORAC levels in diabetic rats.
|