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镉诱导的肠病:氯化镉与镉硫蛋白的比较毒性

Cadmium-induced enteropathy: comparative toxicity of cadmium chloride and cadmium-thionein.

作者信息

Valberg L S, Haist J, Cherian M G, Delaquerriere-Richardson L, Goyer R A

出版信息

J Toxicol Environ Health. 1977 Mar;2(4):963-75. doi: 10.1080/15287397709529495.

Abstract

In protecting the body against the noxious effects of dietary cadmium ions, cadmium is bound to metallothionein in the proximal intestine, and subsequently excreted into the lumen with desquamation of the epithelium. The purpose of this study was to determine the extent to which cadmium in the form of intestinal cadmium-thionein is absorbed from the intestinal lumen and to appraise the toxicity of cadmium-thionein on the intestinal mucosa. With open-ended duodenal perfusion, equivalent amounts of cadmium administered as CdCl2 or cadmium-thionein entered the mucosa, but significantly less cadmium from the perfusate of cadmium-thionein passed into the body. Exposure of the mucosa to CdCl2 for 1 hr led to minor abnormalities in the form of broadening of villi with pseudostratification of epithelium, and swelling of mitochondria, whereas cadmium-thionein produced extensive necrosis of absorptive cells. The results suggest that cadmium-thionein may play a paradoxical role, providing protection against the cadmium ion in the intracellular milieu, but promoting cadmium toxicity when it is present in sufficient amounts in the lumen of the intestine.

摘要

为保护机体免受膳食镉离子的有害影响,镉在近端肠道与金属硫蛋白结合,随后随着上皮细胞的脱落而排泄到肠腔中。本研究的目的是确定肠镉 - 硫蛋白形式的镉从肠腔吸收的程度,并评估镉 - 硫蛋白对肠黏膜的毒性。采用开放式十二指肠灌注,以氯化镉或镉 - 硫蛋白形式给予等量的镉进入黏膜,但来自镉 - 硫蛋白灌注液的镉进入体内的量明显较少。黏膜暴露于氯化镉1小时会导致轻微异常,表现为绒毛增宽伴上皮假复层形成以及线粒体肿胀,而镉 - 硫蛋白则导致吸收细胞广泛坏死。结果表明,镉 - 硫蛋白可能发挥矛盾的作用,在细胞内环境中提供对镉离子的保护,但当它在肠腔中大量存在时会促进镉的毒性。

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