Coenzyme Q, oxidative stress and aging

Coenzyme Q (CoQ) has three well-characterized functions in mitochondria, namely (i) transfer of reducing equivalents in the electron transport chain, (ii) generation of superoxide anion radical, O₂^{{radical dot} -}, and (iii) quenching of free radicals. The main purpose of this review is to discuss the effects of CoQ₁₀ intake for relatively prolonged periods on mitochondrial respiratory capacity, indicators of oxidative stress, and life span of animals, in context of the broader issue of whether or not the overall progression of the aging process can be modified by CoQ₁₀ administration. Comparative studies on different mammalian species have indicated that the rate of mitochondrial superoxide anion radical generation is directly correlated with mitochondrial CoQ₉ content and inversely related to amounts of CoQ₁₀, particularly the CoQ₁₀ bound to mitochondrial membrane proteins. Contrary to the historical view, dietary supplementation of mice and rats with CoQ₁₀ has been demonstrated to augment the endogenous CoQ content (CoQ₉ + CoQ₁₀) in mitochondria and homogenates of various tissues, albeit to varying extent. Ingestion of CoQ₁₀ results in the elevation of endogenous CoQ₉, the predominant homologue in mice and rats. In our studies, there was no indication of a discernable effect of CoQ₁₀ intake reflecting enhancement of mitochondrial respiratory activity, antioxidant capacity and pro-oxidant potentiation or prolongation of life span. The possibility that CoQ₁₀ intake affects certain other biological functions by as yet unelucidated mechanisms cannot be ruled out as CoQ has been shown to broadly alter gene expression in mice.