Abstract
The hormetic effect, which extends lifespan by various stressors, has been confirmed in Caenorhabditis elegans (C. elegans). We have previously reported that oxidative stress resistance in a long-lived mutant age-1 is associated with the hormesis. In an age-1 allele that activates an intracellular insulin/insulin-like growth factor-1 (Ins/IGF-1) signaling pathway, the superoxide dismutase (SOD) and catalase activities increased during normal aging. We now demonstrate the changes of mitochondrial superoxide radical (.O2-) levels in age-related strains under a hormetic condition. The .O2- levels in age-1 strain significantly decreased after intermittent hyperoxia exposure. On the other hand, this phenomenon was not observed in a daf-16 null mutant. This hormesis-dependent reduction of the .O2- levels was observed even if the mitochondrial Mn-SOD was experimentally reduced. Therefore, it is indicated that the hormesis is mediated by any event suppressing the mitochondrial .O2- production. Moreover, we describe change in the oxygen consumption levels of the age-1 mutant in the oxygen radical-induced hormesis. The oxygen consumption levels in age-1 animal significantly decreased after intermittent hyperoxia exposure. These data suggest that oxidative stress-inducible hormesis is associated with reduction of mitochondrial .O2- production by activation of an antioxidant system via Ins/IGF-1 signaling pathway.
