Energy metabolism, anti-oxidant defense and aging in Caenorhabditis elegans

Abstract

Food restriction and impaired gene function by mutation or RNAi treatment can extend the lifespan of Caenorhabditis elegans considerably. In contrast to the widespread belief, the antiaging action of these interventions is not due to a reduction of the rate of metabolism. Calorie restriction causes several alterations that are similar to those observed for the Ins/IGF mutants, but acts independently of this pathway. Life extension is associated with coordinated increases in superoxide dismutase and catalase activities in calorie-restricted worms and in mutants in the Ins/IGF transduction pathway. Mutation in any one of the clk genes does not result in a clear metabolic downregulation or upregulation of antioxidant enzymes. Lifespan extension in these mutants might be linked to their slow developmental rate during juvenile life, analogous to the effects caused by silencing of several genes with a mitochondrial function by RNAi treatment, and suggesting a regulatory system that makes various rates of juvenile life to persist during adulthood. The outcome would be slowing of a number of processes during adulthood, including aging.