title: Adaptive responses to oxidative damage in three mutants of Caenorhabditis elegans (age-1, mev-1 and daf-16) that affect life span.
abstract: Oxidative damage shortens the life span of the nematode Caenorhabditis elegans (C. elegans), even in an age-1 mutant that is characterized by a long life and oxygen resistance. We found that daily short-term exposure (3 h) to hyperoxia further extended the life span of age-1, a phenomenon known as an adaptive response. age-1 also showed resistance to paraquat and heat. Acute hyperoxic treatment did not extend the life spans of wild type, daf-16 or mev-1. daf-16 mutant had a slightly shorter life span compared to wild type and was sensitive to heat and paraquat. The daf-16 phenotype resembles that of mev-1 showing a short life and oxygen sensitivity. We measured mRNA levels of superoxide dismutase genes (sod-1 through 4), catalase genes (clt-1 and ctl-2), known to encode anti-oxidant enzymes, and found they were elevated in age-1 young adults. On the other hand, in daf-16 and mev-1, the expression of sod-1, sod-2 and sod-3 genes was lower rather than in wild type. Conversely, ctl-1 and ctl-2 genes expression was significantly elevated in daf-16 and mev-1. This suggests that DAF-16, a forkhead/winged-helix transcription factor, whose expression is suppressed by AGE-1, phosphoinositide 3-kinase (PI3-kinase), regulates anti-oxidant genes as well as energy metabolism under atmospheric conditions. However, the level of gene expression of SOD and catalase was not elevated by short-term exposure to 90% oxygen in wild type, mev-1, daf-16 and even age-1. This suggests that SOD and catalase do not play a role in the adaptive response against oxidative stress under hyperoxia, at least under these experimental conditions.
authors.affiliation: Department of Molecular Life Science, Tokai University School of Medicine, Boseidai, Isehara, Kanagawa 259-1193, Japan.
authors.forename: Sumino
authors.initials: S
authors.lastname: Yanase
authors.forename: Kayo
authors.initials: K
authors.lastname: Yasuda
authors.forename: Naoaki
authors.initials: N
authors.lastname: Ishii
mesh_terms: D000222:Adaptation, Physiological / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001833:Body Temperature Regulation / Q000502:physiology; D017173:Caenorhabditis elegans / Q000235:genetics*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism; D002374:Catalase / Q000235:genetics; D003580:Cytochromes / Q000235:genetics / Q000378:metabolism; D045303:Cytochromes b; D051858:Forkhead Transcription Factors; D008136:Longevity / Q000235:genetics*; D009154:Mutation / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D010100:Oxygen / Q000378:metabolism / Q000494:pharmacology; D010641:Phenotype; D019869:Phosphatidylinositol 3-Kinases; D013482:Superoxide Dismutase / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: D000975:Antioxidants; D029742:Caenorhabditis elegans Proteins; D003580:Cytochromes; D051858:Forkhead Transcription Factors; C472666:MEV-1 protein, C elegans; D014157:Transcription Factors; C108831:daf-16 protein, C elegans; D045303:Cytochromes b; D002374:Catalase; D013482:Superoxide Dismutase; D019869:Phosphatidylinositol 3-Kinases; C100662:AGE-1 protein, C elegans; D010100:Oxygen