A role for reduced coenzyme Q in atherosclerosis?

Substantial evidence implicates oxidative modification of low density lipoprotein (LDL) as an important event contributing to atherogenesis. As a result, the elucidation of the molecular mechanisms by which LDL is oxidized and how such oxidation is prevented by antioxidants has been a significant research focus. Studies on the antioxidation of LDL lipids have focused primarily onα‐tocopherol (α‐TOH), biologically and chemically the most active form of vitamin E and quantitatively the major lipid‐soluble antioxidant in extracts prepared from human LDL. In addition toα‐TOH, plasma LDL also contains low levels of ubiquinol‐10 (CoQ 10 H 2 ; the reduced form of coenzyme Q 10 ). Recent studies have shown that in oxidizing plasma lipoproteinsα‐TOH can exhibit anti‐ or pro‐oxidant activities for the lipoprotein's lipids exposed to a vast array of oxidants. This article reviews the molecular action ofα‐TOH in LDL undergoing “mild” radical‐initiated lipid peroxidation, and discusses how small levels of CoQ 10 H 2 can represent an efficient antioxidant defence for lipoprotein lipids. We also comment on the levelsα‐TOH, CoQ 10 H 2 and lipid oxidation products in the intima of patients with coronary artery disease and report on preliminary studies examining the effect of coenzyme Q 10 supplementation on atherogenesis in apolipoprotein E knockout mice.