Oxidative stress and cell cycle checkpoint function

被引:430
|
作者
Shackelford, RE
Kaufmann, WK
Paules, RS
机构
[1] NIEHS, Growth Control & Canc Grp, Res Triangle Pk, NC 27709 USA
[2] Univ N Carolina, Dept Pathol & Lab Med, Chapel Hill, NC USA
[3] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA
关键词
reactive oxygen species; oxidative stress; DNA damage; cell cycle; checkpoints; free radicals;
D O I
10.1016/S0891-5849(00)00224-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Oxidative stress and the damage that results from it have been implicated in a wide number of disease processes including atherosclerosis, autoimmune disorders, neuronal degeneration, and cancer. Reactive oxygen species (ROS) are ubiquitous and occur naturally in all aerobic species, coming from both exogenous and endogenous sources. ROS are quite reactive and readily damage biological molecules, including DNA. While the damaging effects of ROS on DNA have been intensively studied, the effects of oxidative damage on cell cycle checkpoint function have not. Here will we review several biologically important ROS and their sources, the cell cycle, checkpoints, and current knowledge about the effects of ROS on initiating checkpoint responses. (C) 2000 Elsevier Science Inc.
引用
收藏
页码:1387 / 1404
页数:18
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