A role for reduced coenzyme Q in atherosclerosis?

Article type: Research Article

Authors: Thomas, Shane R. | Witting, Paul K. | Stocker, Roland

Affiliations: The Biochemistry Group, The Heart Research Institute, 145 Missenden Road, Camperdown, NSW 2050, Australia Tel.: +61 2 9550 3560; Fax: +61 2 9550 3302; E‐mail: r.stocker@ hri.org.au

Abstract: 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 on \alpha‐tocopherol (\alpha‐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 to \alpha‐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 lipoproteins \alpha‐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 of \alpha‐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 levels \alpha‐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.

Journal: Biofactors, vol. 9, no. 2-4, pp. 207-224, 1999