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Research: THOMAS and colleagues, Bi
Listed in Issue 32
Abstract
THOMAS and colleagues, Biochemistry Unit, Heart Research Institute, Sydney New South Wales, Australia write that oxidation of low density lipoprotein (LDL) is now regarded as a key early event in atherogenesis, hence explaining the interest in the ability of antioxidant supplementation to attenuate LDL oxidation and therefore, possibly atherosclerosis.
Background
Methodology
The authors write that the majority of studies regarding LDL antioxidation have focused upon alpha-tocopherol (alpha-TOH), the most active form, biologically and chemically, of vitamin E, and the major lipid-soluble antioxidant in extracts prepared from human LDL.
Results
Circulating LDL also contains, in addition to alpha-TOH, low levels of ubiquinol-10 (CoQ10H2 the reduced form of coenzyme Q). Research with intact, isolated LDL has demonstrated that alpha-TOH can act as either an anti- or prooxidant for the lipoproteins lipids. The authors review (70 references) the literature regarding the molecular action of alpha-TOH in LDL undergoing radical-initiated oxidation and how CoQ10H2 suppresses the pro-oxidant or complements the antioxidant activity of vitamin E. They also comment on the plasma and intimal levels of alpha-TOH and CoQ10H2 in patients with coronary artery disease and discuss the potential implications of this research regarding atherogenesis.
Conclusion
References
Thomas SR et al. Inhibition of LDL oxidation by ubiquinol-10. A protective mechanism for coenzyme Q in atherogenesis? Mol Aspects Med. 18 (Supp): S85-103. 1997.
Comment
Recently it was published that vitamin C can act as both as a pro- as well as an anti-oxidant. The above study shows that vitamin E can do the same, and that CoQ10 can act in cooperation with vitamin E to suppress LDL oxidation.
