Against the oxidative damage theory of aging: superoxide dismutases protect against oxidative stress but have little or no effect on life span in Caenorhabditis elegans

  1. Ryan Doonan1,3,
  2. Joshua J. McElwee1,3,
  3. Filip Matthijssens2,3,
  4. Glenda A. Walker1,
  5. Koen Houthoofd2,
  6. Patricia Back2,
  7. Andrea Matscheski1,
  8. Jacques R. Vanfleteren2, and
  9. David Gems1,4
  1. 1 Institute of Healthy Ageing and Research Department of Genetics, Evolution and Environment, University College London, London WC1E 6BT, United Kingdom;
  2. 2 Department of Biology, Ghent University, B-9000 Ghent, Belgium

  1. ↵3 These authors contributed equally to this work.

Abstract

The superoxide radical (O2−) has long been considered a major cause of aging. O2− in cytosolic, extracellular, and mitochondrial pools is detoxified by dedicated superoxide dismutase (SOD) isoforms. We tested the impact of each SOD isoform in Caenorhabditis elegans by manipulating its five sod genes and saw no major effects on life span. sod genes are not required for daf-2 insulin/IGF-1 receptor mutant longevity. However, loss of the extracellular Cu/ZnSOD sod-4 enhances daf-2 longevity and constitutive diapause, suggesting a signaling role for sod-4. Overall, these findings imply that O2− is not a major determinant of aging in C. elegans.

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  1. doi: 10.1101/gad.504808 Genes & Dev. 22: 3236-3241 Copyright © 2008, Cold Spring Harbor Laboratory Press

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