Testing the rate-of-living/oxidative damage theory of aging in the nematode model Caenorhabditis elegans.

The integration of the rate-of-living and oxidative damage theory of aging predicts that lifespan extension is linked to low energy metabolism, low ROS production rates, low molecular damage and a slow aging rate. In the long-lived Caenorhabditis elegans Ins/IGF-1 mutant daf-2(e1370), low carbonylation levels and postponed morphological decline comply with the latter two of these predictions. However, metabolic rates in daf-2(e1370) refute the rate-of-living theory. The apparent contradiction between increased ROS generation and long lifespan in daf-2(e1370) is reconciled by an enhanced stress defense, acknowledging oxidative damage as a probable cause of aging.