Schriner Samuel E, Linford Nancy J, Martin George M, Treuting Piper, Ogburn Charles E, Emond Mary, Coskun Pinar E, Ladiges Warren, Wolf Norman, Van Remmen Holly, Wallace Douglas C, Rabinovitch Peter S
Department of Genome Sciences, University of Washington, Seattle, WA 91895, USA.
Science. 2005 Jun 24;308(5730):1909-11. doi: 10.1126/science.1106653. Epub 2005 May 5.
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.
为了确定活性氧在哺乳动物寿命中的作用，我们构建了过表达定位于过氧化物酶体、细胞核或线粒体的人过氧化氢酶的转基因小鼠（MCAT）。MCAT小鼠的平均寿命和最长寿命均显著延长（分别平均延长5个月和5.5个月）。心脏病理变化和白内障发展延缓，氧化损伤减轻，过氧化氢生成及过氧化氢诱导的乌头酸酶失活减弱，线粒体缺失的发生减少。这些结果支持衰老的自由基理论，并强化了线粒体作为这些自由基来源的重要性。
