Journal
GENES & DEVELOPMENT
Volume 22, Issue 23, Pages 3236-3241Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.504808
Keywords
Aging; Caenorhabditis elegans; free radical; superoxide dismutase; insulin/IGF-1 signaling; genetics
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Funding
- Wellcome Trust and the European Union
- Ghent University [GOA 12050101]
- Fund for Scientific Research-Flanders [G.0025.06]
- European Community [LSHM-CT-2004512020]
- Institute for the Promotion of Innovation by Science and Technology in Flanders (IWT)
- National Institutes of Health National Center for Research Resources
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The superoxide radical (O-2(-)) has long been considered a major cause of aging. O-2(-) 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 O-2(-) is not a major determinant of aging in C. elegans.
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