Atorvastatin increases blood ratios of vitamin E/low-density lipoprotein cholesterol and coenzyme Q10/low-density lipoprotein cholesterol in hypercholesterolemic patients.
Statins are among the most widely used drugs in the management of hypercholesterolemia. In addition to inhibiting endogenous cholesterol synthesis, however, statins decrease coenzyme Q10 (CoQ10) synthesis. CoQ10 has been reported to have antioxidant properties, and administration of drugs that decrease CoQ10 synthesis might lead to increased oxidative stress in vivo. Our present study examined the hypothesis that atorvastatin increased oxidative stress in hypercholesterolemic patients due to its inhibition of CoQ10 synthesis. We investigated the effects of atorvastatin (10 mg/d) administration for 5 months on lowering hypercholesterolemia and blood antioxidant status. The study population included 19 hypercholesterolemic outpatients. Blood levels of lipid and antioxidant markers, consisting of vitamin C, vitamin E, CoQ10, and glutathione (GSH), and urinary levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) were examined pre- and postadministration of atorvastatin. Atorvastatin administration resulted in a significant decrease in blood levels of total cholesterol, triglycerides, low-density lipoprotein (LDL) cholesterol, vitamin E, and CoQ10 (P < .05); however, a significant increase in the ratios of vitamin E/LDL cholesterol and CoQ10/LDL cholesterol was noted (P < .05). Atorvastatin had no significant effect on red blood cell (RBC) level of GSH and urinary 8-OHdG. The present study provides evidence that atorvastatin exerts a hypocholesterolemic effect, but on the basis of the urinary level of 8-OHdG and the blood ratios of vitamin E/LDL cholesterol and CoQ10/LDL cholesterol, has no oxidative stress-inducing effect.
Department of Neurology, Changhua Christian Hospital, Changhua, Taiwan.
Chin-San
CS
Liu
Chong-Kuei
CK
Lii
Li-Ling
LL
Chang
Chen-Ling
CL
Kuo
Wen-Ling
WL
Cheng
Shih-Li
SL
Su
Chia-Wen
CW
Tsai
Haw-Wen
HW
Chen
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000368:Aged; D000924:Anticholesteremic Agents / Q000009:adverse effects* / Q000627:therapeutic use; D000069059:Atorvastatin; D008078:Cholesterol, LDL / Q000097:blood*; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D005978:Glutathione / Q000097:blood; D006538:Heptanoic Acids / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D006937:Hypercholesterolemia / Q000188:drug therapy*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D011758:Pyrroles / Q000009:adverse effects* / Q000627:therapeutic use; D014451:Ubiquinone / Q000031:analogs & derivatives* / Q000096:biosynthesis / Q000097:blood; D014810:Vitamin E / Q000097:blood*
D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D008055:Lipids; D011758:Pyrroles; D014451:Ubiquinone; D014810:Vitamin E; D000080242:8-Hydroxy-2'-Deoxyguanosine; D000069059:Atorvastatin; C024989:coenzyme Q10; D003849:Deoxyguanosine; D005978:Glutathione