Lieven Christopher J, Vrabec Joshua P, Levin Leonard A
Antioxid Redox Signal. 2003 Oct;5(5):641-6. doi: 10.1089/152308603770310310.
Retinal ganglion cells (RGCs) are central neurons that undergo apoptosis after axonal injury. As the relationship between mitochondrial and oxidative signaling of apoptosis in neuronal systems is unclear, we sought to achieve a better understanding of the interplay of these two pathways by investigating the effect of direct oxidative stress on mitochondrial membrane potential in cultured RGCs, as measured with the dual-emission probe JC-1. Treatment with hydrogen peroxide caused RGC mitochondrial depolarization. Several pharmacological treatments were used to define the mechanism. Whereas cycloheximide, tris(2-carboxyethyl)phosphine, and cyclosporin A were unable to prevent the depolarization, bongkrekic acid significantly reduced the severity of the depolarization. This suggests that the hydrogen peroxide-induced depolarization may act through mitochondrial permeability transition pore opening independent of thiol oxidation, and may be preventable under certain conditions.
视网膜神经节细胞（RGCs）是中枢神经元，轴突损伤后会发生凋亡。由于神经元系统中线粒体与凋亡的氧化信号之间的关系尚不清楚，我们试图通过研究直接氧化应激对培养的RGCs线粒体膜电位的影响（用双发射探针JC-1测量），来更好地理解这两条途径之间的相互作用。过氧化氢处理导致RGC线粒体去极化。使用了几种药理学处理方法来确定其机制。虽然环己酰亚胺、三（2-羧乙基）膦和环孢素A无法阻止去极化，但米酵菌酸显著降低了去极化的严重程度。这表明过氧化氢诱导的去极化可能通过线粒体通透性转换孔开放起作用，与硫醇氧化无关，并且在某些条件下可能是可预防的。
