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A role for reduced coenzyme Q in atherosclerosis?
Author(s) -
Thomas Shane R.,
Witting Paul K.,
Stocker Roland
Publication year - 1999
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520090216
Subject(s) - coenzyme q – cytochrome c reductase , cardiology , chemistry , medicine , biochemistry , cytochrome c , mitochondrion
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.