Overexpression of Mn superoxide dismutase does not increase life span in mice

Youngmok C. Jang, Viviana I. Pérez, Wook Song, Michael S. Lustgarten, Adam B. Salmon, James Mele, Wenbo Qi, Yuhong Liu, Hanyu Liang, Asish Chaudhuri, Yuji Ikeno, Charles J. Epstein, Holly Vanremmen, Arlan G Richardson

Research output: Contribution to journalArticlepeer-review

145 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1114-1125
Number of pages12
JournalJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Issue number11
StatePublished - 2009


  • Aging
  • Mn superoxide dismutase
  • Oxidative damage
  • Pathology

ASJC Scopus subject areas

  • Aging
  • Geriatrics and Gerontology


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