Inhibition of LDL oxidation by ubiquinol-10. A protective mechanism for coenzyme Q in atherogenesis?

Abstract

The oxidation of low density lipoprotein (LDL) is now commonly regarded as an important early event in atherogenesis. As such there is considerable interest in the ability of antioxidant supplementation to attenuate LDL oxidation and hence atherosclerosis. A majority of studies on LDL antioxidation have focused on α-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 to α-TOH, circulating LDL also contains low levels of ubiquinol-10 (CoQ 10H 2; the reduced form of coenzyme Q). Recent studies have shown that in intact, isolated LDL, α-TOH can act as either an anti- or pro-oxidant for the lipoprotein's lipids. This article reviews the molecular action of α-TOH in LDL undergoing radical-initiated oxidation, and how the presence of CoQ 10H 2 supresses the pro-oxidant or complements the antioxidant activity of the vitamin. We also comment on the plasma and intimal levels of α-TOH and CoQ 10H 2 in patients suffering from coronary artery disease and discuss the potential implications of these results for atherogenesis.