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锌对大鼠氯化汞毒性的保护机制:锌和汞对谷胱甘肽代谢的影响。

Mechanism of protection by zinc against mercuric chloride toxicity in rats: effects of zinc and mercury on glutathionine metabolism.

作者信息

Fukino H, Hirai M, Hsueh Y M, Moriyasu S, Yamane Y

出版信息

J Toxicol Environ Health. 1986;19(1):75-89. doi: 10.1080/15287398609530908.

Abstract

To investigate the mechanism by which zinc suppresses mercury toxicity, the effects of zinc and mercury on glutathione (GSH) metabolism in the rat kidney were studied. When the time course of GSH level in the rat kidney was examined at 2, 6, and 12 h after treatment of rats with both metals, an increase of GSH was found and was apparently related to the activation of some GSH-associated enzymes. In the kidney of rats treated with both metals, the response of the protective function involving GSH and GSH-associated enzymes depended on the magnitude of mercury toxicity but appeared to be independent of the zinc dosage. The administration of diethyl maleate (DEM), which depletes GSH, increased lipid peroxidation and mercury toxicity concomitantly with a decrease of GSH level in the kidney of rats treated with zinc and mercury. In conclusion, the data suggest that an increased GSH level in the kidney resulting from the activation of GSH-associated enzymes plays a role in the protective effect of zinc against mercury toxicity.

摘要

为研究锌抑制汞毒性的机制,对锌和汞对大鼠肾脏中谷胱甘肽(GSH)代谢的影响进行了研究。当在两种金属处理大鼠后2、6和12小时检查大鼠肾脏中GSH水平的时间进程时,发现GSH增加,这显然与一些GSH相关酶的激活有关。在同时用两种金属处理的大鼠肾脏中,涉及GSH和GSH相关酶的保护功能反应取决于汞毒性的大小,但似乎与锌剂量无关。给予耗尽GSH的马来酸二乙酯(DEM),会增加脂质过氧化和汞毒性,同时在用锌和汞处理的大鼠肾脏中GSH水平降低。总之,数据表明,由GSH相关酶激活导致的肾脏中GSH水平升高在锌对汞毒性的保护作用中发挥作用。

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