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

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 a...

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Bibliographic Details
Published in:The journals of gerontology. Series A, Biological sciences and medical sciences Biological sciences and medical sciences, 2009-11, Vol.64A (11), p.1114-1125
Main Authors: Jang, Youngmok C., Pérez, Viviana I., Song, Wook, Lustgarten, Michael S., Salmon, Adam B., Mele, James, Qi, Wenbo, Liu, Yuhong, Liang, Hanyu, Chaudhuri, Asish, Ikeno, Yuji, Epstein, Charles J., Van Remmen, Holly, Richardson, Arlan
Format: Article
Language:English
Subjects:
Aging
Aging - metabolism
Animals
Effects
Enzymes
Female
Gene expression
Genetics
Journal of Gerontology: Biological Sciences
Male
Mice
Mice, Inbred C57BL
Mice, Transgenic
Mitochondria, Muscle - physiology
Mn superoxide dismutase
Muscle, Skeletal - pathology
Organ Size
Oxidation
Oxidative damage
Oxidative Stress
Pathology
Reactive Oxygen Species - metabolism
Rodents
Superoxide Dismutase - physiology
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Summary: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.
ISSN:1079-5006
1758-535X
DOI:10.1093/gerona/glp100