Oxidative modification of proteins during aging
Oxidative modification of proteins during aging
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DOI：
10.1016/s0531-5565(01)00135-8
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发表时间：
2001-09-01
影响因子：
3.9
通讯作者：
Stadtman, ER
中科院分区：
文献类型：
--
作者：
Levine, RL;Stadtman, ER
越来越多的实验证据支持这样一种观点：衰老过程中发生的许多变化是氧化损伤的结果。活性氧与所有三种主要的细胞大分子、核酸、脂质和蛋白质发生反应。这篇综述的重点是在衰老过程中作为氧化物质靶点的蛋白质。许多由这些氧化物质介导的反应导致羰基进入蛋白质。从秀丽隐杆线虫到人类，含羰基蛋白的稳态水平在生命的最后三分之一呈指数增长。延长寿命的遗传和非遗传操作导致蛋白质羰基水平的下降，而缩短寿命的操作则增加了水平。含有羰基的氧化蛋白通常是功能失调的，在生命的最后三分之一，这些氧化蛋白的含量上升到可能导致细胞功能实质性破坏的水平。Elsevier Science Inc.出版。
Accumulating experimental evidence supports the proposal that many of the changes which occur during aging are a consequence of oxidative damage. Reactive oxygen species react with all three of the major cellular macromolecules, nucleic acids, lipids, and proteins. This minireview focuses on proteins as targets of oxidizing species during aging. Many of the reactions mediated by these oxidizing species result in the introduction of carbonyl groups into proteins. The steady-state level of carbonyl-bearing proteins increases exponentially during the last third of lifespan in animals ranging from C. elegans to man. Genetic and non-genetic manipulations which lengthen lifespan cause a decrease in the level of protein carbonyl while those which shorten lifespan increase the level. Oxidized proteins bearing carbonyl groups are generally dysfunctional, and in the last third of lifespan the content of these oxidized proteins rises to a level likely to cause substantial disruption of cellular function. Published by Elsevier Science Inc.