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
Year: 2008
Type: article
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.
Source: Journal of Radiation Research
DOI: 10.1269/jrr.07043
Authors: Sumino YANASE, Naoaki ISHII
Institutions: Tokai University, Daito Bunka University
Language: English
Subfield: Aging
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,430
OpenAlex ID: W2118989234
