The role of ubiquinone in Caenorhabditis elegans longevity

Aging is an irreversible physiological process that affects all living organisms. Different mutations in the insulin signaling pathway and caloric restriction have been shown to retard aging in Caenorhabditis elegans. In addition, mutations or RNAi silencing of components of the respiratory chain results in the modification of adult life span. Another class of genes that affect life span in C. elegans is the clock (clk) genes. Particularly interesting is clk-1, which encodes an enzyme required for ubiquinone (coenzyme Q, CoQ) biosynthesis. Down-regulation by RNAi silencing of the genes required for ubiquinone biosynthesis also extends life span in C. elegans, and CoQ supplied in the diet also affects nematode longevity in both clk-1 and wild-type strains. Although there are many aspects that can be considered in aging, we focus this review on the role of CoQ in the longevity of C. elegans. We will review the current information about the biosynthesis of CoQ and its dietary supplementation related to the extension of life span. We will also analyze the function of CoQ in the electron transport chain and reactive oxygen species production in the context of aging. We hypothesize that the role of CoQ on longevity of C. elegans supports the oxidative damage theory of aging.