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首页> 外文期刊>Life sciences >Mechanism of ethanol enhancement of apoptosis and caspase activation in serum-deprived PC12 cells.
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Mechanism of ethanol enhancement of apoptosis and caspase activation in serum-deprived PC12 cells.

机译：乙醇增强血清剥夺的PC12细胞凋亡和caspase活化的机制。

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Neuronal death is one of the most prominent consequences of alcohol exposure during development. Ethanol-induced neuronal death appears to involve apoptosis. The objective of the present study was to characterize the effect of ethanol on neuronal cell viability and to determine the mechanism by which ethanol enhances apoptosis in neural cells. For these studies the rat pheochromocytoma (PC12) cells were used. PC12 cells were incubated for 24 h in the presence or absence of 100 mM ethanol. Apoptosis was induced by serum withdrawal. Ethanol in the presence of serum-containing media did not alter cell viability, while incubation of PC12 cells in serum-free media resulted in a significant increase in cell death that was further significantly increased by 35% in cells exposed to ethanol. The temporal response of the PC12 cells to serum withdrawal was studied over a period of 22 h. At least 18 h of ethanol exposure was necessary to observe a significant increase in death for cells incubated in serum-free media. An increase in the caspase-3 activity in PC12 cells deprived of serum was observed that was further increased by ethanol exposure. This increase of caspase-3 activity was correlated with an enhancement of caspase-9 activity. Ethanol exposure increased the amount of cytosolic cytochrome c in PC12 cells incubated in serum-free media but did not alter the level of cytochrome c in cells incubated in serum. Finally, a 26% increase was observed in the number of cells with depolarized mitochondria due to ethanol treatment. The present study implicates an increase in the mitochondrial outer membrane permeability as a potential mechanism of enhancement of apoptosis in serum-deprived PC12 cells by ethanol.
机译：神经元死亡是发育过程中酒精暴露的最突出后果之一。乙醇诱导的神经元死亡似乎与细胞凋亡有关。本研究的目的是表征乙醇对神经元细胞活力的影响，并确定乙醇增强神经细胞凋亡的机制。为了进行这些研究，使用了大鼠嗜铬细胞瘤（PC12）细胞。在存在或不存在100 mM乙醇的情况下，将PC12细胞孵育24小时。血清停药诱导细胞凋亡。在含血清的培养基中存在乙醇不会改变细胞活力，而在无血清的培养基中孵育PC12细胞会导致细胞死亡的显着增加，而在暴露于乙醇的细胞中则进一步显着增加35％。在22小时内研究了PC12细胞对血清戒断的时间反应。要在无血清培养基中培养的细胞观察到死亡的显着增加，必须至少暴露18小时的乙醇。观察到缺乏血清的PC12细胞中caspase-3活性的增加通过乙醇暴露而进一步增加。 caspase-3活性的这种增加与caspase-9活性的增强相关。乙醇暴露会增加在无血清培养基中孵育的PC12细胞中胞质细胞色素c的量，但不会改变在血清中孵育的细胞中细胞色素c的水平。最后，由于乙醇处理，线粒体去极化的细胞数量增加了26％。本研究暗示线粒体外膜通透性的增加是乙醇增强血清剥夺的PC12细胞凋亡的潜在机制。

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