Superoxide dismutase is dispensable for normal animal lifespan
- 26 March 2012
- journal article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences of the United States of America
- Vol. 109 (15), 5785-5790
- https://doi.org/10.1073/pnas.1116158109
Abstract
Reactive oxygen species (ROS) are toxic oxygen-containing molecules that can damage multiple components of the cell and have been proposed to be the primary cause of aging. The antioxidant enzyme superoxide dismutase (SOD) is the only eukaryotic enzyme capable of detoxifying superoxide, one type of ROS. The fact that SOD is present in all aerobic organisms raises the question as to whether SOD is absolutely required for animal life and whether the loss of SOD activity will result in decreased lifespan. Here we use the genetic model organism Caenorhabditis elegans to generate an animal that completely lacks SOD activity (sod-12345 worms). We show that sod-12345 worms are viable and exhibit a normal lifespan, despite markedly increased sensitivity to multiple stresses. This is in stark contrast to what is observed in other genetic model organisms where the loss of a single sod gene can result in severely decreased survival. Investigating the mechanism underlying the normal lifespan of sod-12345 worms reveals that their longevity results from a balance between the prosurvival signaling and the toxicity of superoxide. Overall, our results demonstrate that SOD activity is dispensable for normal animal lifespan but is required to survive acute stresses. Moreover, our findings indicate that maintaining normal stress resistance is not crucial to the rate of aging.This publication has 41 references indexed in Scilit:
- The Homeobox Protein CEH-23 Mediates Prolonged Longevity in Response to Impaired Mitochondrial Electron Transport Chain in C. elegansPLoS Biology, 2011
- A Mitochondrial Superoxide Signal Triggers Increased Longevity in Caenorhabditis elegansPLoS Biology, 2010
- Inhibition of Respiration Extends C. elegans Life Span via Reactive Oxygen Species that Increase HIF-1 ActivityCurrent Biology, 2010
- Deletion of the Mitochondrial Superoxide Dismutase sod-2 Extends Lifespan in Caenorhabditis elegansPLoS Genetics, 2009
- Against the oxidative damage theory of aging: superoxide dismutases protect against oxidative stress but have little or no effect on life span in Caenorhabditis elegansGenes & Development, 2008
- Modulation of longevity and diapause by redox regulation mechanisms under the insulin-like signaling control in Caenorhabditis elegansExperimental Gerontology, 2008
- 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 elegansGenetics, 2007
- Trends in oxidative aging theoriesFree Radical Biology & Medicine, 2007
- Superoxide Dismutase Activity Is Essential for Stationary Phase Survival in Saccharomyces cerevisiae: MITOCHONDRIAL PRODUCTION OF TOXIC OXYGEN SPECIES IN VIVOOnline Journal of Public Health Informatics, 1996
- Aging: A Theory Based on Free Radical and Radiation ChemistryJournal of Gerontology, 1956