The free-radical hypothesis of aging goes prokaryotic.

Abstract

With respect to oxidative damage and its targets, growth-arrested bacterial cells show some of the same signs of senescence as aging insects, worms and mammals. In addition, the fact that the life span of growth-arrested Escherichia coli cells is greatly extended by limiting oxygen availability suggests that free radicals may be one causal factor behind bacterial senescence. Recent analysis reveals a novel culprit in this oxidation, namely the production of aberrant proteins, which are especially susceptible to oxidative attack. This route of oxidation appears to elude the classical oxidative defense proteins. In addition, the failure of growth-arrested cells to fully combat oxidative damage may be linked to a trade-off between proliferation activities and stress management. Even during stasis, E. coli cells maintain a basal transcription of reproduction-related genes, and resources are thus partly diverted from maintenance and stress defences to activities relating to proliferation. Thus, some aspects of bacterial senescence may lend support to contemporary theories of aging, including the free radical, antagonistic pleiotropy, and disposable soma theories.