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Mitochondrial hormesis was a purely hypothetical concept until late 2007, when work by Michael Ristow's group on a small worm named Caenorhabditis elegans suggested that the restriction of glucose metabolism extends life span primarily by increasing oxidative stress to stimulate the organism into having an ultimately increased resistance to further oxidative stress.[61] This is probably the first experimental evidence for hormesis being the reason for extended life span following CR. Although aging can be conceptualized as the accumulation of damage, the more recent determination that free radicals participate in intracellular signaling has made the categorical equation of their effects with "damage" more problematic than was commonly appreciated in the past. It was previously proposed on a hypothetical basis that free radicals may induce an endogenous response culminating in more effective adaptations that protect against exogenous radicals (and possibly other toxic compounds).[74] Recent experimental evidence strongly suggests that this is indeed the case, and that such induction of endogenous free-radical production extends the life span of a model organism and mitohormetically exerts life-extending and health-promoting effects. Sublethal mitochondrial stress with an attendant stoichiometric augmentation of reactive oxygen species may precipitate many of the beneficial alterations in cellular physiology produced by caloric restriction.[75][76][77] |
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