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證明老化與氧化關系的重要研究
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"Extension of murine lifespan by overexpression of catalase targeted to mitochondria." Science, 308:1909-11, 2005. 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. Department of Genome Sciences, University of Washington, Seattle, WA 91895, USA. 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 mitochondrial deletions was reduced. These results support the free radical theory of aging and reinforce the importance of mitochondria as a source of these radicals. The finding: Peter Rabinovitch at the University of Washington at Seattle and his colleagues found that transgenic mice overexpressing the antioxidant enzyme catalase in their mitochondria lived nearly 20% longer and exhibited less heart disease and other age-related declines. This supported the free-radical theory of aging. |
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2楼2007-03-23 07:47:47