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HeLa细胞中金属硫蛋白生成的调控

Regulation of metallothionein production in HeLa cells.

作者信息

Koizumi S, Sone T

机构信息

Department of Experimental Toxicology, National Institute of Industrial Health, Kawasaki, Japan.

出版信息

Toxicol Lett. 1991 Dec;59(1-3):73-80. doi: 10.1016/0378-4274(91)90057-d.

Abstract

Metallothioneins are cysteine-rich, heavy-metal-binding proteins which have been assumed to participate in the detoxification of toxic metals. The mechanism of thionein (apoprotein of metallothionein) induction by cadmium was studied using cultured human cells. It was found that when thionein synthesis reaches a maximum (6-8 h after induction), it no longer responds to additional cadmium. Changes in cadmium uptake or induction of inhibitory proteins were not responsible. Together with our previous findings, a possible mechanism is proposed: loss of the secondary induction response might be due to increased intracellular levels of thionein, which has been overproduced by the initial induction.

摘要

金属硫蛋白是富含半胱氨酸的重金属结合蛋白,被认为参与有毒金属的解毒过程。利用培养的人类细胞研究了镉诱导硫蛋白(金属硫蛋白的脱辅基蛋白)的机制。结果发现,当硫蛋白合成达到最大值时(诱导后6 - 8小时),它不再对额外的镉产生反应。镉摄取的变化或抑制蛋白的诱导并不是原因所在。结合我们之前的发现,提出了一种可能的机制:二次诱导反应的丧失可能是由于细胞内硫蛋白水平的增加,而硫蛋白是由最初的诱导过度产生的。

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