Chromosomal DNA fragmentation in apoptosis and necrosis induced by oxidative stress
Chromosomal DNA fragmentation in apoptosis and necrosis induced by oxidative stress
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DOI：
10.1016/s0006-2952(03)00508-2
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发表时间：
2003-10-15
影响因子：
5.8
通讯作者：
Higuchi, Y
中科院分区：
文献类型：
--
作者：
Higuchi, Y
染色体DNA功能障碍在哺乳动物细胞死亡中起着重要作用。氧化应激产生的活性氧(ROS)导致染色质功能障碍，如单链和双链DNA断裂，通过细胞凋亡或坏死导致细胞死亡。在多种哺乳动物细胞的凋亡或坏死过程中，氧化应激和某些产生ROS的因素可产生超过1MBP的巨型DNA、200-800或50-300KBP的高分子量DNA和核小体间DNA片段。对参与染色体DNA断裂的一些核酸酶进行了分类。ROS介导的DNA断裂是由多不饱和脂肪酸(PUFAs)或其氢过氧化通过脂质过氧化引起和加强的。抑制半胱氨酸转运或GSH生物合成导致细胞内GSH水平降低，从而导致某些哺乳动物细胞中ROS的过量产生和积累，从而导致细胞死亡。ROS积累系统已被用作氧化应激的模型，以讨论ROS介导的与细胞死亡相关的DNA断裂是基于细胞凋亡还是基于坏死。(C)2003 Elsevier Inc.保留所有权利。
Chromosomal DNA dysfunction plays a role in mammalian cell death. Oxidative stress producing reactive oxygen species (ROS) induces chromatin dysfunction such as single- and double-strand DNA fragmentation leading to cell death through apoptosis or necrosis. More than 1 Mbp giant DNA, 200-800 or 50-300 kbp high molecular weight (HMW) DNA and internucleosomal DNA fragments are produced by oxidative stress and by some agents producing ROS during apoptosis or necrosis in several types of mammalian cells. Some nucleases involved in the chromosomal DNA fragmentation in apoptosis or necrosis are classified. ROS-mediated DNA fragmentation is caused and enhanced by polyunsaturated fatty acids (PUFAs) or their hydroperoxides through lipid peroxidation. A reduction of intracellular GSH levels induced by the inhibition of cystein transport or GSH biosynthesis leads to cell death through over production and accumulation of ROS in some types of mammalian cells. The ROS accumulation system has been used as a model of oxidative stress to discuss whether ROS-mediated DNA fragmentation associated with cell death is based on apoptosis or necrosis. (C) 2003 Elsevier Inc. All rights reserved.