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

doi:10.1093/gerona/glp100

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

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160 Scopus citations

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.

Original language	English (US)
Pages (from-to)	1114-1125
Number of pages	12
Journal	Journals of Gerontology - Series A Biological Sciences and Medical Sciences
Volume	64
Issue number	11
DOIs	https://doi.org/10.1093/gerona/glp100
State	Published - 2009

Keywords

Aging
Mn superoxide dismutase
Oxidative damage
Pathology

ASJC Scopus subject areas

General Medicine

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Jang, Y. C., Pérez, V. I., Song, W., Lustgarten, M. S., Salmon, A. B., Mele, J., Qi, W., Liu, Y., Liang, H., Chaudhuri, A., Ikeno, Y., Epstein, C. J., Vanremmen, H., & Richardson, A. G. (2009). Overexpression of Mn superoxide dismutase does not increase life span in mice. Journals of Gerontology - Series A Biological Sciences and Medical Sciences, 64(11), 1114-1125. https://doi.org/10.1093/gerona/glp100

Jang, YC, Pérez, VI, Song, W, Lustgarten, MS, Salmon, AB, Mele, J, Qi, W, Liu, Y, Liang, H, Chaudhuri, A, Ikeno, Y, Epstein, CJ, Vanremmen, H & Richardson, AG 2009, 'Overexpression of Mn superoxide dismutase does not increase life span in mice', Journals of Gerontology - Series A Biological Sciences and Medical Sciences, vol. 64, no. 11, pp. 1114-1125. https://doi.org/10.1093/gerona/glp100

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title = "Overexpression of Mn superoxide dismutase does not increase life span in mice",

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 = "Aging, Mn superoxide dismutase, Oxidative damage, Pathology",

author = "Jang, {Youngmok C.} and P{\'e}rez, {Viviana I.} and Wook Song and Lustgarten, {Michael S.} and Salmon, {Adam B.} and James Mele and Wenbo Qi and Yuhong Liu and Hanyu Liang and Asish Chaudhuri and Yuji Ikeno and Epstein, {Charles J.} and Holly Vanremmen and Richardson, {Arlan G}",

note = "Funding Information: National Institutes of Health grants (P01AG19316, P01AG020591, R37AG026557 to A.R.), the San Antonio Nathan Shock Aging Center ( 1P30-AG13319 VA Merit grants (A.R. and H.V.R.) and the Reserve Educational Assistance Program from the Department of Veteran Affairs .",

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T1 - Overexpression of Mn superoxide dismutase does not increase life span in mice

AU - Jang, Youngmok C.

AU - Pérez, Viviana I.

AU - Song, Wook

AU - Lustgarten, Michael S.

AU - Salmon, Adam B.

AU - Mele, James

AU - Qi, Wenbo

AU - Liu, Yuhong

AU - Liang, Hanyu

AU - Chaudhuri, Asish

AU - Ikeno, Yuji

AU - Epstein, Charles J.

AU - Vanremmen, Holly

AU - Richardson, Arlan G

N1 - Funding Information: National Institutes of Health grants (P01AG19316, P01AG020591, R37AG026557 to A.R.), the San Antonio Nathan Shock Aging Center ( 1P30-AG13319 VA Merit grants (A.R. and H.V.R.) and the Reserve Educational Assistance Program from the Department of Veteran Affairs .

PY - 2009

Y1 - 2009

N2 - 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.

AB - 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.

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KW - Mn superoxide dismutase

KW - Oxidative damage

KW - Pathology

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

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