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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences Advance Access originally published online on July 24, 2009
The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 2009 64A(11):1114-1125; doi:10.1093/gerona/glp100
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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.

Overexpression of Mn Superoxide Dismutase Does Not Increase Life Span in Mice

Youngmok C. Jang1,2, Viviana I. Pérez1,2, Wook Song1,2, Michael S. Lustgarten2,3, Adam B. Salmon2, James Mele2,3, Wenbo Qi1,2, Yuhong Liu1,2, Hanyu Liang1,2, Asish Chaudhuri2,4,5, Yuji Ikeno1,2,5, Charles J. Epstein6, Holly Van Remmen1,2,5 and Arlan Richardson1,2,5

1 Department of Cellular and Structural Biology
2 The Sam and Ann Barshop Institute for Longevity and Aging Studies
3 Department of Physiology
4 Department of Biochemistry, University of Texas Health Science Center at San Antonio
5 GRECC, South Texas Veterans Health Care System, San Antonio
6 Institute of Human Genetics and Department of Pediatrics, University of California, San Francisco

Address correspondence to Arlan Richardson, PhD, The Sam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, 15355 Lambda Drive, San Antonio, TX 78245-3207. Email: richardsona{at}uthscsa.edu


  Abstract

Genetic manipulations of Mn superoxide dismutase (MnSOD), SOD2 expression have demonstrated that altering the level of MnSOD activity is critical for cellular function and life span in invertebrates. In mammals, Sod2 homozygous knockout mice die shortly after birth, and alterations of MnSOD levels are correlated with changes in oxidative damage and in the generation of mitochondrial reactive oxygen species. In this study, we directly tested the effects of overexpressing MnSOD in young (4–6 months) and old (26–28 months) mice on mitochondrial function, levels of oxidative damage or stress, life span, and end-of-life pathology. Our data show that an approximately twofold overexpression of MnSOD throughout life in mice resulted in decreased lipid peroxidation, increased resistance against paraquat-induced oxidative stress, and decreased age-related decline in mitochondrial ATP production. However, this change in MnSOD expression did not alter either life span or age-related pathology.

Keywords Oxidative damage; Mn superoxide dismutase; Pathology; Aging

Received: November 13, 2008; Accepted: July 1, 2009

Decision Editor: Huber R. Warner, PhD


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