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镉暴露大鼠肝脏和肾脏金属硫蛋白生物合成的机制

The mechanisms of hepatic and renal metallothionein biosynthesis in cadmium-exposed rats.

作者信息

Shaikh Z A, Smith J C

出版信息

Chem Biol Interact. 1977 Nov;19(2):161-71. doi: 10.1016/0009-2797(77)90028-x.

Abstract

The mechanisms by which cadmium (Cd) stimulates the synthesis of hepatic and renal metallothionein were investigated in rats. In the liver the incorporation of 35S and 14C labels from cystine showed a lag period of about 2 h and maximum incorporation into metallothionein took place 8--12 h after injection of 30 mumol CdCl2/kg. The incorporation of the labels into renal metallothionein was faster than into the hepatic protein; the lag period was less than 1 h and maximum incorporation occurred 4--5 h after the Cd injection. Cycloheximide inhibited the amino acid incorporation into both hepatic and renal metallothionein. Actinomycin D treatment, however, inhibited hepatic metallothionein synthesis only. These results suggested that at the dose level employed Cd regulated the biosynthesis of metallothionein in the liver at the transcriptional level and in the kidney at the translational level.

摘要

研究了镉(Cd)刺激大鼠肝脏和肾脏金属硫蛋白合成的机制。在肝脏中,胱氨酸的35S和14C标记掺入显示约2小时的延迟期,注射30 μmol CdCl2/kg后8 - 12小时金属硫蛋白的掺入量达到最大。标记物掺入肾脏金属硫蛋白的速度比掺入肝脏蛋白的速度快;延迟期小于1小时,Cd注射后4 - 5小时掺入量达到最大。环己酰亚胺抑制氨基酸掺入肝脏和肾脏金属硫蛋白。然而,放线菌素D处理仅抑制肝脏金属硫蛋白的合成。这些结果表明,在所采用的剂量水平下,Cd在转录水平调节肝脏中金属硫蛋白的生物合成,在翻译水平调节肾脏中金属硫蛋白的生物合成。

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