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氢过氧化异丙苯对水蛭Retzius神经细胞的毒性作用:谷胱甘肽的保护作用

Toxicity induced by cumene hydroperoxide in leech Retzius nerve cells: the protective role of glutathione.

作者信息

Jovanovic Zorica, Jovanovic Svetlana

机构信息

Department ofPathophysiology, Faculty of Medicine, Kragujevac, Republic of Serbia.

出版信息

Folia Biol (Krakow). 2013;61(1-2):93-100. doi: 10.3409/fb61_1-2.93.

DOI:10.3409/fb61_1-2.93
PMID:23767299
Abstract

In the present study, we studied the ability of glutathione (GSH) to detoxify exogenously applied cumene hydroperoxide (CHP). Exposure of leech Retzius nerve cells to CHP (1.5 mM) induced a marked prolongation of the spontaneous spike potential of these cells. Early after depolarization, and a cardiac-like action potential with a rapid depolarization followed by a sustained depolarization or plateau, which is terminated by a rapid repolarization were recorded. GSH (0.2 mM) significantly inhibited the effects of CHP on the duration of the action potential and suppressed CHP-induced spontaneous repetitive activity. Voltage-clamp recordings showed that CHP (1.5 mM) caused significant changes in the outward potassium currents. The fast and slow steady part of the potassium outward current was reduced by 46% and 39%, respectively. GSH applied in a concentration of 0.2 mM partially blocked the effect of CHP on the calcium-activated potassium currents. The fast and slow calcium-activated potassium currents were suppressed by about 20% and 15%, respectively. These results suggest that the neurotoxic effect of CHP on spontaneous spike electrogenesis and calcium-activated potassium currents of leech Retzius nerve cells was reduced in the presence of GSH.

摘要

在本研究中,我们研究了谷胱甘肽(GSH)对外源性施加的氢过氧化异丙苯(CHP)的解毒能力。将水蛭雷特修斯神经细胞暴露于CHP(1.5 mM)会导致这些细胞的自发尖峰电位显著延长。去极化后早期,记录到一种类似心脏的动作电位,其快速去极化后接着是持续去极化或平台期,并由快速复极化终止。GSH(0.2 mM)显著抑制了CHP对动作电位持续时间的影响,并抑制了CHP诱导的自发重复活动。电压钳记录显示,CHP(1.5 mM)导致外向钾电流发生显著变化。钾外向电流的快速和缓慢稳定部分分别降低了46%和39%。浓度为0.2 mM的GSH部分阻断了CHP对钙激活钾电流的影响。快速和缓慢的钙激活钾电流分别被抑制了约20%和15%。这些结果表明,在存在GSH的情况下,CHP对水蛭雷特修斯神经细胞自发尖峰电活动和钙激活钾电流的神经毒性作用降低。

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