期刊
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
卷 64, 期 11, 页码 1114-1125出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/glp100
关键词
Oxidative damage; Mn superoxide dismutase; Pathology; Aging
资金
- National Institutes of Health [P01AG19316, P01AG020591, R37AG026557]
- San Antonio Nathan Shock Aging Center [1P30-AG13319]
- VA Merit grants
- Department of Veteran Affairs
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据