Mitochondria and the regulation of free radical damage in the eye.
Mitochondria and the regulation of free radical damage in the eye.
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DOI：
10.1007/s12177-009-9036-4
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发表时间：
2009-09
期刊：
影响因子：
--
通讯作者：
Barnstable CJ
中科院分区：
文献类型：
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作者：
Barnstable CJ
神经元细胞死亡可以通过由外源性来源和作为氧化磷酸化副产物的内源性产物的组合产生的活性氧（ROS）的总体水平来确定。ROS内在产生的关键控制者是线粒体解偶联蛋白（UCPs）。通过允许受控的质子泄漏穿过线粒体内膜，这些蛋白质的活化可以减少ROS并促进细胞存活。在帕金森病的灵长类动物模型和癫痫发作的小鼠模型中，UCP2活性的增加显著增加了神经元细胞的存活。在视网膜中，UCP2在许多神经元和神经胶质细胞中表达，但在视杆细胞中未检测到。兴奋性毒性损伤后视网膜神经节细胞的存活率在UCP2过表达的动物中要高得多。传统中药，如管花肉苁蓉提取物，可能通过改变线粒体代谢提供益处。
Neuronal cell death can be determined by the overall level of reactive oxygen species (ROS) resulting from the combination of extrinsic sources and intrinsic production as a byproduct of oxidative phosphorylation. Key controllers of the intrinsic production of ROS are the mitochondrial uncoupling proteins (UCPs). By allowing a controlled leak of protons across the inner mitochondrial membrane activation of these proteins can decrease ROS and promote cell survival. In both primate models of Parkinson’s disease and mouse models of seizures, increased activity of UCP2 significantly increased neuronal cells survival. In the retina UCP2 is expressed in many neurons and glial cells, but was not detected in rod photoreceptors. Retinal ganglion cell survival following excitotoxic damage was much greater in animals overexpressing UCP2. Traditional Chinese medicines, such as an extract of Cistanche tubulosa, may provide benefit by altering mitochondrial metabolism.