Hormetic effect induced a longevity in <i>C. elegans</i> is due to the changes of oxygen consumption and superoxide radical production.

DOI
  • YANASE Sumino
    Daito Bunka University, School of Sports & Health Science Tokai University, School of Medicine, Department of Life Science
  • SHOUYAMA Tetsuji
    Tokai University, School of High-Technology for Human Welfare, Department of Biological Science and Technology
  • SUDA Hitoshi
    Tokai University, School of High-Technology for Human Welfare, Department of Biological Science and Technology
  • ISHII Naoaki
    Tokai University, School of Medicine, Department of Life Science

Bibliographic Information

Other Title
  • 線虫<i>C. elegans</i>における寿命延長を誘発するホルミシス効果は、ミトコンドリア呼吸鎖における酸素消費量およびラジカル産生量の変化に起因する

Search this article

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 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, the expressions at the mRNA levels of some SOD gene in age-1 mutant under a hormetic condition were induced from the steady state. These data suggest that oxidative stress-inducible hormesis is associated with a reduction of mitochondrial .O2- production by activation of an antioxidant system via Ins/IGF-1 signaling pathway.

Journal

Keywords

Details 詳細情報について

Report a problem

Back to top