EXOGENOUS COQ(10) PRESERVES PLASMA UBIQUINONE LEVELS IN PATIENTS TREATED WITH 3-HYDROXY-3-METHYLGLUTARYL COENZYME-A REDUCTASE INHIBITORS

Ubiquinone is a carrier of the mitochondrial respiratory chain which r egulates oxidative phosphorylation: it also acts as a membrane stabili zer preventing lipid peroxidation. In man the quinone ring originates from tyrosine, while the formation of the polyisoprenoid lateral chain starts from acetyl CoA and proceeds through mevalonate and isopenteny lyprophosphate; this biosynthetic pathway is the same as the cholester ol one. We therefore performed this study to evaluate whether statins (hypocholesterolemic drugs that inhibit 3-hydroxy-3-methylglutaryl coe nzyme A reductase) modify blood levels of ubiquinone. Thirty unrelated outpatients with primary hypercholesterolemia (IIa phenotype) were tr eated with 20 mg of simvastatin for a 3-month period (group S) or with 20 mg of simvastatin plus 100 mg CoQ(10) (group US). The following pa rameters were evaluated at time 0, and at 45 and 90 days: total plasma cholesterol, high-density lipoprotein-cholesterol, low-density lipopr otein-cholesterol, triglycerides, Apo A1, Apo B and CoQ(10) in plasma and in platelets. In the S group, there was a marked decrease in total cholesterol low-density lipoprotein-cholesterol and in plasma CoQ(10) levels from 1.08 mg/dl to 0.80 mg/dl. In contrast, in the US group we observed a significant increase of plasma CoQ(10) (from 1.20 to 1.48 mg/dl) while the hypocholesterolemic effect was similar to that observ ed in the S group. Platelet CoQ(10) also decreased in the S group (fro m 104 to 90 ng/mg) and increased in the US group (from 95 to 145 ng/mg ). This study demonstrated that simvastatin lowered both low-density l ipoprotein-cholesterol and Apo B plasma levels and plasma and platelet levels of CoQ(10), and that CoQ(10) prevent both plasma and platelet CoQ(10) reduction, without affecting the hypocholesterolemic effect of simvastatin.