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镉或锌诱导的金属硫蛋白可抑制暴露于二甲基亚硝胺的大鼠体内的脂质过氧化。

Metallothionein induced by cadmium or zinc inhibits lipid peroxidation in rats exposed to dimethylnitrosamine.

作者信息

Rana S V, Kumar A

机构信息

Department of Zoology, Ch. Charan Singh University, Meerut, India.

出版信息

Arh Hig Rada Toksikol. 2000 Sep;51(3):279-86.

Abstract

Dimethylnitrosamine (N-nitrosodimethyamine) is a potent inducer of microsomal lipid peroxidation in the liver and kidneys. The results of this study show that prior exposure of adult rats to cadmium or zinc antagonises the effect of dimethylnitrosamine on lipid peroxidation by inducing increased metallothionein synthesis. Increased concentration of reduced glutathione (GSH) in the liver and kidney of rats pre-treated with cadmium or zinc and exposed to dimethylnitrosamine suggests that metallothionein inhibits oxidative stress. The presented results have been corroborated by findings that exposure of adult rats to cadmium or zinc may activate genes for metallothionein and glutathione-S-transferase, the protective proteins against oxidative stress.

摘要

二甲基亚硝胺(N-亚硝基二甲胺)是肝脏和肾脏中微粒体脂质过氧化的强效诱导剂。本研究结果表明,成年大鼠预先接触镉或锌可通过诱导金属硫蛋白合成增加来拮抗二甲基亚硝胺对脂质过氧化的影响。在预先用镉或锌处理并接触二甲基亚硝胺的大鼠的肝脏和肾脏中,还原型谷胱甘肽(GSH)浓度增加,这表明金属硫蛋白可抑制氧化应激。成年大鼠接触镉或锌可能会激活金属硫蛋白和谷胱甘肽-S-转移酶的基因,这两种都是抗氧化应激的保护蛋白,这一发现证实了上述结果。

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