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

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  • YANASE Sumino
    Department of Health Science, Daito Bunka University School of Sports & Health Science Department of Molecular Life Science, Tokai University School of Medicine
  • ISHII Naoaki
    Department of Molecular Life Science, Tokai University School of Medicine

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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 (·O2-) levels of the hormetic conditioned age-related strains. 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 events that suppress the mitochondrial ·O2- 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 ·O2- production by activation of the antioxidant system via the Ins/IGF-1 signaling pathway.

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