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1 is of glutathione, phospholipids, NADPH, and coenzyme Q10.
2 OQ2 and is essential for the biosynthesis of coenzyme Q10.
3 ebral cortex mitochondrial concentrations of coenzyme Q10.
4 wed that TQ is reduced more efficiently than coenzyme Q10.
5 eatine, 66 received minocycline, 71 received coenzyme Q10, 71 received GPI-1485, and 138 received pla
11 ched control subjects and that the levels of coenzyme Q10 and the activities of complex I and complex
15 we have identified 6 different mutations in coenzyme Q10 biosynthesis monooxygenase 6 (COQ6) in 13 i
16 mutations in genes that function within the coenzyme Q10 biosynthesis pathway, suggesting that SRNS
17 omparison of the rate of reduction of TQ and coenzyme Q10 by NQO1 showed that TQ is reduced more effi
22 investigated whether oral administration of coenzyme Q10 (CoQ10) could attenuate 1-methyl-4-phenyl-1
24 The authors performed sequencing of known Coenzyme Q10 (CoQ10) deficiency genes in 22 patients wit
25 irst described in 1989, our understanding of coenzyme Q10 (CoQ10) deficiency is only now coming of ag
29 Here we report the important role of the coenzyme Q10 (CoQ10) on the activity of caspase-2 upstre
30 ence available for oral supplementation with coenzyme Q10 (CoQ10) to improve the tolerability of canc
32 evented the adverse effects of alcohol while coenzyme Q10 (CoQ10) was not very effective against alco
33 stnatal supplementation with the antioxidant coenzyme Q10 (CoQ10) would prevent this programmed pheno
40 pe B inhibitors (selegiline and rasagiline), coenzyme Q10, creatine, and exercise in early Parkinson'
41 are due to defects in nuclear DNA, including coenzyme Q10 deficiency and mutations in genes controlli
43 eficiency, and one patient was found to have coenzyme Q10 deficiency due to compound heterozygous mut
44 are due to defects in nuclear DNA, including coenzyme Q10 deficiency, and mutations in genes that con
49 ough the mean (+/-SD) serum concentration of coenzyme Q10 increased from 0.95+/-0.62 microg/mL to 2.2
50 ese results show that oral administration of coenzyme Q10 increases both brain and brain mitochondria
55 cronutrients involved in cardiac metabolism: coenzyme Q10, l-carnitine, thiamine, and amino acids, in
58 We found that oral administration of either coenzyme Q10 or remacemide significantly extended surviv
59 ductase 1, NADH-ferrocyanide reductase, NADH-coenzyme Q10 reductase, and NADH-cytochrome c reductase)
62 mutations had lower coenzyme Q10 levels, and coenzyme Q10 supplementation ameliorated renal disease i
63 Therapeutic trials of exercise training and coenzyme Q10 supplementation should continue to be offer
64 lls lacking MFN2 can be partially rescued by coenzyme Q10 supplementation, which suggests a possible
68 ects of an antioxidant mixture of vitamin A, coenzyme Q10, vitamin C, and vitamin E were evaluated fo
69 A was more effective than ascorbic acid, and Coenzyme Q10 was more effective than vitamin E acetate.
72 decanoic acid) and lipophilic nutraceutical (Coenzyme Q10) was investigated using a rat feeding study
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