摘要
青光眼是一种多因素诱导的视神经退行性病变，其中氧化应激损伤在复杂的青光眼发病机制中的起着重要作用。青光眼的氧化损伤机制可能对眼部的某些组织细胞产生损伤作用，促使细胞内抗氧化物酶作用下降、抗氧化作用相关蛋白增加，最终导致蛋白沉积、细胞死亡。氧化损伤可以导致小梁网细胞线粒体骨架改变，最终使小梁网发生退行性病理改变。氧化损伤还可促使视网膜神经节细胞内抗氧化作用相关蛋白增加、线粒体内源性凋亡，最终导致视网膜神经节细胞功能丧失。（国际眼科纵览，2013，37：59—62）
Glaucoma is an irreversible neuropathy and oxidative stress probably plays an important role in its pathological process. Oxidative damage can destroy cells of many parts of ocular tissue, induce de- crease of intracellular antioxidant enzymes and increase antioxidant-related proteins, finally lead to deposition of these proteins and cell death. Oxidative damage also modifies the cytoskeleton of mitochondria in trabecu- lar meshwork cells and causes pathologic degradation of trabecular meshwork ceils. Oxidative stress also in- duces raise of antioxidant-related proteins and endogenous apoptosis of mitochondria in retinal ganglion cells, and lastly results in retinal ganglion cell dysfunction. （Int Rev Ophthalmol, 2013, 37：59-62 ）
出处
《国际眼科纵览》
2013年第1期59-62,共4页
International Review of Ophthalmology
