Apoptosis induced in neuronal cells by oxidative stress: role played by caspases and intracellular calcium ions
Apoptosis induced in neuronal cells by oxidative stress: role played by caspases and intracellular calcium ions
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DOI：
10.1016/s0378-4274(02)00427-7
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发表时间：
2003-04-04
影响因子：
3.5
通讯作者：
Di Renzo, GF
中科院分区：
文献类型：
--
作者：
Annunziato, L;Amoroso, S;Di Renzo, GF
活性氧（ROS）参与了许多神经系统疾病和脑功能障碍的病理生理学。在相同的病理环境中，已经提供了有利于细胞内Ca 2+浓度改变稳态参与导致神经元凋亡的事件链的证据。本文综述了caspase激活与细胞内钙离子浓度变化在神经元凋亡机制中的关系，并对相关文献报道和实验数据进行了讨论。收集的数据支持这样的结论：在神经元细胞的氧化应激期间，活性氧的产生触发了一种机制，通过线粒体释放细胞色素c和半胱天冬酶-3激活，导致细胞凋亡;伴随的活性氧介导的细胞内Ca 2+浓度升高触发了半胱天冬酶-2激活，但这两种事件似乎并不参与细胞死亡。(C)2002爱思唯尔科学爱尔兰有限公司保留所有权利。
Reactive oxygen species (ROS) have been implicated in the pathophysiology of many neurologic disorders and brain dysfunction. In the same pathological settings evidence has been provided in favour of a participation of intracellular Ca2+ concentration altered homeostasis in the chain of events leading to neuronal apoptosis. In the present review literature reports and experimental data on the relationship between caspase activation and alteration of intracellular calcium concentrations in the mechanisms triggering neuronal apoptosis are discussed. The data gathered support the conclusion that during oxidative stress in neuronal cells the production of ROS triggers a mechanism that, through the release of cytochrome c from mitochondria and caspase-3 activation, leads to apoptosis; the concomitant ROS-mediated elevation of intracellular Ca2+ concentration triggers caspase-2 activation but both events do not seem to be involved in cell death. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.