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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences Advance Access published online on March 12, 2009
The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, doi:10.1093/gerona/glp020
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© The Author 2009. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

SOD-1 Deletions in Caenorhabditis elegans Alter the Localization of Intracellular Reactive Oxygen Species and Show Molecular Compensation

Sumino Yanase1,2, Akira Onodera2, Patricia Tedesco3, Thomas E. Johnson3 and Naoaki Ishii2

1 Department of Health Science, Daito Bunka University School of Sports and Health Science, Saitama, Japan
2 Department of Molecular Life Science, Tokai University School of Medicine, Kanagawa, Japan
3 Institute for Behavioral Genetics, University of Colorado at Boulder

Address correspondence to Naoaki Ishii, PhD, Department of Molecular Life Science, Tokai University School of Medicine, Bohseidai, Isehara, Kanagawa 259-1193, Japan. Email: nishii{at}is.icc.u-tokai.ac.jp


  Abstract

SUPEROXIDE dismutase (SOD) is an enzyme that catalytically removes the superoxide radical () and protects organisms from oxidative damage during normal aging. We demonstrate that not only the cytosolic level but also the mitochondrial level increases in the deletion mutants of sod-1 gene encoding Cu/Zn SOD in Caenorhabditis elegans (C. elegans). Interestingly, this suggests that the activity of SOD-1, which so far has been thought to act mainly in cytoplasm, helps to control the detoxification of also in the mitochondria. We also found functional compensation by other SODs, especially the sod-5 gene, which was induced several fold in the mutants. Therefore, the possibility exists that the compensative expression of sod-5 gene in the sod-1 deficit is associated with the insulin/insulin-like growth factor-1 (Ins/IGF-1) signaling pathway, which regulates longevity and stress resistance of C. elegans because the sod-5 gene may be a target of the pathway.

Keywords Sod-1; Sod-5; Mitochondrial ROS production; Oxidative stress; Aging

Received: May 11, 2008; Accepted: July 8, 2008

Decision Editor: Huber R. Warner, PhD


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