Extension of murine life span by overexpression of catalase targeted to mitochondria

被引:1289
作者
Schriner, SE
Linford, NJ
Martin, GM
Treuting, P
Ogburn, CE
Emond, M
Coskun, PE
Ladiges, W
Wolf, N
Van Remmen, H
Wallace, DC
Rabinovitch, PS [1 ]
机构
[1] Univ Washington, Dept Pathol, Seattle, WA 98195 USA
[2] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA
[3] Univ Washington, Dept Comparat Med, Seattle, WA 98195 USA
[4] Univ Washington, Dept Biostat, Seattle, WA 98195 USA
[5] Univ Calif Irvine, Ctr Mol & Mitochondrial Med & Genet, Dept Biol Chem, Irvine, CA 92697 USA
[6] Univ Calif Irvine, Dept Ecol & Evolut Biol, Irvine, CA 92697 USA
[7] Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA
关键词
D O I
10.1126/science.1106653
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
To determine the, role of reactive oxygen species in mammalian longevity, we generated transgenic mice that overexpress human catalase localized to the peroxisome, the nucleus, or mitochondria (MCAT). Median and maximum life spans were maximally increased (averages of 5 months and 5.5 months, respectively) in MCAT animals. Cardiac pathology and cataract development were delayed, oxidative damage was reduced, H2O2 production and H2O2-induced aconitase inactivation were attenuated, and the development of mitochondria) deletions was reduced. These results support the free radical theory of aging and reinforce the importance of mitochondria as a source of these radicals.
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收藏
页码:1909 / 1911
页数:3
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