Authors: Yanase, Sumino; Ishii, Naoaki
Abstract: The hormetic effect, which extends the 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 the age-1 allele, which activates an 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 changes in the mitochondrial superoxide radical (*O(2)(-)) levels of the hormetic conditioned age-related strains. The *O(2)(-) 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 *O(2)(-) levels was observed even if the mitochondrial Mn-SOD was experimentally reduced. Therefore, it is indicated that the hormesis is mediated by events that suppress the mitochondrial *O(2)(-) production. Moreover, some SOD gene expressions in the hormetic conditioned age-1 mutant were induced over steady state mRNA levels. These data suggest that oxidative stress-inducible hormesis is associated with a reduction of the mitochondrial *O(2)(-) production by activation of the antioxidant system via the Ins/IGF-1 signaling pathway.
Keywords: Animals; Caenorhabditis elegans/genetics/physiology; Caenorhabditis elegans Proteins/*genetics; Insulin/*physiology; Insulin-Like Growth Factor I/*physiology; Longevity/physiology; Mitochondria/*chemistry; Mutation; Phosphatidylinositol 3-Kinases/*genetics; Signal Transduction/*physiology; Superoxides/*analysis|
Journal: J Radiat Res Volume: 49 Issue: 3 Pages: 211-8 Date: Feb. 21, 2008 PMID: 18285659 |
Yanase, Sumino, Ishii, Naoaki (2008) Hyperoxia exposure induced hormesis decreases mitochondrial superoxide radical levels via Ins/IGF-1 signaling pathway in a long-lived age-1 mutant of Caenorhabditis elegans. J Radiat Res 49: 211-8.
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