Cytochrome C is released from mitochondria into the cytosol after cerebral anoxia or ischemia
Cytochrome C is released from mitochondria into the cytosol after cerebral anoxia or ischemia
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DOI：
10.1097/00004647-199901000-00004
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发表时间：
1999-01-01
影响因子：
6.3
通讯作者：
Sick, TJ
中科院分区：
文献类型：
--
作者：
Pérez-Pinzón, MA;Xu, GP;Sick, TJ
线粒体功能障碍可能是脑缺血引起的急性和迟发性神经细胞死亡的基础。具体而言，缺血后释放的线粒体成分，如促凋亡呼吸链组分细胞色素c可以急性进一步线粒体功能障碍，并促进迟发性神经元死亡。本文报道的实验验证了缺血或严重缺氧导致线粒体释放细胞色素c的假设。细胞色素c是从全脑缺血加再灌注后皮质脑匀浆的胞浆部分，或从严重缺氧加复氧的脑切片中通过荧光定量法测定的。缺血再灌注后，大脑皮质细胞液中细胞色素c含量增加。在完整的海马切片中，缺氧/复氧后可还原的细胞色素c丢失，这与线粒体池中氧化还原载体的减少一致。这些结果表明，细胞色素c是失去了脑缺血后的方式，可能有助于缺血后线粒体功能障碍和迟发性神经元死亡的细胞质。
Mitochondrial dysfunction may underlie both acute and delayed neuronal cell death resulting from cerebral ischemia. Specifically, postischemic release of mitochondrial constituents such as the pro-apoptotic respiratory chain component cytochrome c could contribute acutely to further mitochondrial dysfunction and to promote delayed neuronal death. Experiments reported here tested the hypothesis that ischemia or severe hypoxia results in release of cytochrome c from mitochondria. Cytochrome c was measured spectrophotometrically from either the cytosolic fraction of cortical brain homogenates after global ischemia plus reperfusion, or from brain slices subjected to severe hypoxia plus reoxygenation. Cytochrome c content in cytosol derived from cerebral cortex was increased after ischemia and reperfusion. In intact hippocampal slices, there was a loss of reducible cytochrome c after hypoxia/reoxygenation, which is consistent with a decrease of this redox carrier in the mitochondrial pool. These results suggest that cytochrome c is lost to the cytosol after cerebral ischemia in a manner that may contribute to postischemic mitochondrial dysfunction and to delayed neuronal death.