ABSTRACT
Among contemporary mechanistic theories of ageing, many view accumulation of molecular damage, particularly oxidative damage, as the primary cause. It has been postulated that a major cause of such damage are reactive oxygen species (ROS), particularly the free radical O2
– (superoxide) and its derivatives (reviewed by Balaban et al., 2005; Raha and Robinson, 2000). O2
– is generated in the cell by diverse processes, for example, as a by-product of the activity of the mitochondrial electron transport chain. Such mitochondrial ROS have been viewed as a possible mechanistic basis of another hypothetical ageing mechanism. The ‘rate of living’ theory postulates that the rate of energy metabolism determines the rate of ageing. It has been suggested that this could be because the rate of production of ROS by mitochondria, and therefore the rate of accrual of molecular damage, is higher when metabolic rate is higher (Sohal and Weindruch, 1996). In the following discussion, I will critically assess in turn whether metabolic rate, mitochondria, and reactive oxygen species are determinants of ageing in the nematode Caenorhabditis elegans. To this end, I will survey the numerous investigations of these issues that have been carried out using this model organism.
