Communication -: Superoxide in apoptosis -: Mitochondrial generation triggered by cytochrome c loss
Communication -: Superoxide in apoptosis -: Mitochondrial generation triggered by cytochrome c loss
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DOI：
10.1074/jbc.273.19.11401
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发表时间：
1998-05-08
影响因子：
4.8
通讯作者：
Jones, DP
中科院分区：
文献类型：
--
作者：
Cai, JY;Jones, DP
细胞凋亡的激活与活性氧的产生有关。目前的研究表明，超氧化物是由线粒体分离的凋亡细胞，由于开关从正常的4-电子还原的O-2，1-电子还原时，细胞色素c从线粒体释放。Bcl-2是一种防止细胞凋亡和阻断细胞色素c释放的蛋白质，当它过度表达时，它会阻止超氧化物的产生。电子转移中的开关提供了伴随细胞色素c依赖的半胱天冬酶激活的氧化还原信号传导机制。细胞色素c释放的阻断为Bcl-2的表观抗氧化功能提供了机制。
Activation of apoptosis is associated with generation of reactive oxygen species. The present research shows that superoxide is produced by mitochondria isolated from apoptotic cells due to a switch from the normal 4-electron reduction of O-2, to a 1-electron reduction when cytochrome c is released from mitochondria. Bcl-2, a protein that protects against apoptosis and blocks cytochrome c release, prevents superoxide production when it is overexpressed. The switch in electron transfer provides a mechanism for redox signaling that is concomitant with cytochrome c-dependent activation of caspases. The block of cytochrome c release provides a mechanism for the apparent antioxidant function of Bcl-2.