Mitochondria and the regulation of free radical damage in the eye.

Colin J Barnstable
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Abstract

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.

Abstract Image

线粒体与眼睛自由基损伤的调节。
神经元细胞的死亡可由外部来源和作为氧化磷酸化副产物的内部产生相结合所产生的活性氧(ROS)的总体水平决定。线粒体解偶联蛋白(UCPs)是 ROS 内在生成的主要控制者。通过控制质子在线粒体内膜上的泄漏,激活这些蛋白可以减少 ROS 并促进细胞存活。在帕金森病灵长类动物模型和癫痫小鼠模型中,UCP2 活性的增加都能显著提高神经细胞的存活率。在视网膜中,UCP2 在许多神经元和神经胶质细胞中都有表达,但在杆状光感受器中没有检测到。过表达 UCP2 的动物在兴奋性毒性损伤后视网膜神经节细胞的存活率更高。中药,如肉苁蓉提取物,可通过改变线粒体代谢而获益。
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