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首页> 外文期刊>Journal of biochemical and molecular toxicology >Thiols and polyamines in the cytoprotective effect of taurine on carbon tetrachloride-induced hepatotoxicity.
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Thiols and polyamines in the cytoprotective effect of taurine on carbon tetrachloride-induced hepatotoxicity.

机译：硫醇和多胺在牛磺酸对四氯化碳诱导的肝毒性的细胞保护作用中。

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摘要

The mechanism by which taurine (2-aminoethanesulfonic acid) protects hepatocytes injury induced by carbon tetrachloride (CCl4) is not fully understood. In a previous study, we reported that cellular polyamines play an important role in this mechanism. The relationship between cellular glutathione (GSH), protein-SH levels, and lactate dehydrogenase (LDH), with respect to the effect of polyamine on the cytoprotective ability of taurine in CCl4-induced toxicity in isolated rat hepatocytes, was examined. CCl4 induced a LDH release and decreased cellular thiols and polyamine levels. Treating with taurine reversed these depletions. The effect of CCl4 was also reversed by the addition of exogenous polyamines. Pretreating with alpha-difluoromethylornithine, an irreversible inhibitor of ornithine decarboxylase, which is a key enzyme in polyamine biosynthesis and therefore used to deplete cellular polyamine, prevented the protective effect of taurine. Adding diethyl maleate, a cellular glutathione-depleting agent, reduced the effect of exogenous polyamines. The role of polyamine in the cytoprotective effect of taurine in CCl4-induced toxicity may therefore be by preventing, among others, GSH and protein-SH depletions.
机译：牛磺酸（2-氨基乙烷磺酸）保护四氯化碳（CCl4）诱导的肝细胞损伤的机制尚不完全清楚。在先前的研究中，我们报道了细胞多胺在该机制中起重要作用。关于多胺对牛磺酸在CCl4诱导的离体大鼠肝细胞毒性中的细胞保护能力的影响方面，研究了细胞谷胱甘肽（GSH），蛋白质SH和乳酸脱氢酶（LDH）之间的关系。 CCl4诱导LDH释放并降低细胞硫醇和多胺水平。用牛磺酸治疗逆转了这些消耗。通过添加外源多胺也可以逆转CCl4的作用。用鸟氨酸脱羧酶的不可逆抑制剂α-二氟甲基鸟氨酸进行预处理，鸟氨酸脱羧酶是多胺生物合成中的关键酶，因此可用于消耗细胞中的多胺，从而阻止了牛磺酸的保护作用。加入马来酸二乙酯（一种细胞内的谷胱甘肽消耗剂）会降低外源多胺的作用。因此，多胺在牛磺酸对CCl4诱导的毒性中的细胞保护作用中的作用可能是通过防止GSH和蛋白质SH耗竭而实现的。

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