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首页> 外文期刊>Apoptosis >Light- and sodium azide-induced death of RGC-5 cells in culture occurs via different mechanisms
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Light- and sodium azide-induced death of RGC-5 cells in culture occurs via different mechanisms

机译：光和叠氮化钠诱导的RGC-5细胞在培养中的死亡通过不同机制发生

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Previous studies have shown that light impinging on the retina in situ has the capacity to kill neuronal and non-neuronal cells in vitro by interacting directly with mitochondrial constituents. A number of fluorophores are associated with mitochondria which can potentially absorb different wave-lengths of light, including cytochrome oxidase. The aim of the present study was to compare the death mechanism of a light insult to RGC-5 cells in culture with that of sodium azide. Sodium azide’s main toxic action is in inhibiting the function of cytochrome oxidase in the mitochondrial electron transport chain. Our studies showed that light and sodium azide kill RGC-5 cells via different mechanisms although some similarities do occur. Both inducers of cell death caused the generation of reactive oxygen species (ROS), the expression of phosphatidylserine, the breakdown of DNA and the activation of p38 MAPK, resulting in its translocation from the nucleus to the cytoplasm. However, light-induced cell death occurs via necroptosis, in that it was inhibited by necrostatin-1 and was caspase-independent. This was not the case for sodium azide, where the death process was caspase-dependent, occurred via apoptosis and was unaffected by necrostatin-1. Moreover, light caused an activation of the apoptosis inducing factor (AIF), c-Jun, JNK and HO-1, but it did not affect alpha fodrin or caspase-3. In contrast, sodium azide caused the activation of alpha fodrin and the stimulation of caspase-3 content without influencing AIF, c-Jun, JNK or HO-1. Therefore we conclude that light does not have a specific action on cytochrome oxidase in mitochondria to cause cell death.
机译：先前的研究表明，入射到视网膜上的光具有通过与线粒体成分直接相互作用而在体外杀死神经元和非神经元细胞的能力。多种荧光团与线粒体相关，可潜在地吸收包括细胞色素氧化酶在内的不同波长的光。本研究的目的是比较轻度损伤培养的RGC-5细胞与叠氮化钠的死亡机理。叠氮化钠的主要毒性作用是抑制线粒体电子传输链中细胞色素氧化酶的功能。我们的研究表明，光和叠氮化钠会通过不同的机制杀死RGC-5细胞，尽管确实存在一些相似之处。两种细胞死亡诱导物均引起活性氧（ROS）的产生，磷脂酰丝氨酸的表达，DNA的分解和p38 MAPK的活化，从而导致其从核转运到细胞质。但是，光诱导的细胞死亡是通过坏死病发生的，因为它被necrostatin-1抑制并且不依赖caspase。叠氮化钠不是这种情况，叠氮化钠的死亡过程是胱天蛋白酶依赖性的，是通过凋亡发生的，不受坏死抑制素-1的影响。此外，光引起细胞凋亡诱导因子（AIF），c-Jun，JNK和HO-1的激活，但它不影响α联蛋白或caspase-3。相比之下，叠氮化钠可引起αfodrin的活化和caspase-3含量的刺激，而不会影响AIF，c-Jun，JNK或HO-1。因此，我们得出结论，光对线粒体中的细胞色素氧化酶没有特异性作用，导致细胞死亡。

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