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Genetics, Vol. 177, 2063-2074, December 2007, Copyright © 2007
doi:10.1534/genetics.107.080788

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A Measurable Increase in Oxidative Damage Due to Reduction in Superoxide Detoxification Fails to Shorten the Life Span of Long-Lived Mitochondrial Mutants of Caenorhabditis elegans

Wen Yang1, Jingjing Li1 and Siegfried Hekimi2

Department of Biology, McGill University, Montreal, Quebec H3A 1B1, Canada

2 Corresponding author: Department of Biology, 1205 Ave. Docteur Penfield, Montreal, Quebec H3A 1B1, Canada.
E-mail: siegfried.hekimi{at}mcgill.ca

SOD-1 and SOD-2 detoxify superoxide in the cytoplasm and mitochondria. We find that, although several long-lived mutants of Caenorhabditis elegans have increased SOD levels, this phenomenon does not correlate with life span or growth rate. Furthermore, although disruption of sod-1 or -2 expression produces numerous phenotypes, including increased sensitivity to paraquat and increased oxidative damage to proteins (except in daf-2 mutants), this fails to shorten the life span of these long-lived mutants. In fact, sod-1(RNAi) increases the life span of daf-2 mutants and sod-2(RNAi) that of clk-1 mutants. Our results suggest that increased superoxide detoxification and low oxidative damage are not crucial for the longevity of the mutants examined, with the possible exception of daf-2, where our results are inconclusive. These results are surprising because several of the long-lived mutants that we examined specifically affect mitochondrial electron transport, a process whose involvement in life-span determination is believed to be related to superoxide generation. We discuss the significance of our findings in light of the oxidative stress theory of aging.






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Copyright © 2007 by the Genetics Society of America.