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肝脏疾病对大鼠体内镉命运的影响。

Effects of hepatic disorder on the fate of cadmium in rats.

作者信息

Tanaka K

出版信息

Dev Toxicol Environ Sci. 1982;9:237-49.

PMID:7053969
Abstract

In order to test the possibility of metallothionein (MT) transfer from liver to kidney, experimental hepatic disorders produced by hepatotoxins were examined to study the release of MT from liver. 109Cd exposed rats were treated with carbon tetrachloride (CCl4) and the distribution of cadmium (Cd) in the body was studied. Hepatic Cd was significantly decreased corresponding to the dose of CCl4. Cd in plasma, kidney, and urine was increased remarkably in contrast with the decrease of hepatic Cd. No remarkable changes in Cd of other tissues and feces were observed. These phenomena were produced by other hepatotoxins like galactosamine and ethionine, and long-term administration of Cd, too. In every case that plasma Cd increased markedly, plasma levels of glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), and lactate dehydrogenase (LDH) rose simultaneously, and a significant, positive correlation between Cd concentration and each of enzyme activities in plasma was observed. Cd in hepatic supernatant of CCl4 treated rats was bound mostly to MT fraction, and in kidney, plasma or urine, Cd was also in the form of MT. These results suggest that hepatic MT can be released into blood in the same manner as hepatic enzymes and transported to kidney and urine in some types of hepatic disorders.

摘要

为了测试金属硫蛋白(MT)从肝脏转移至肾脏的可能性,研究了由肝毒素引起的实验性肝脏疾病,以探讨MT从肝脏的释放情况。用四氯化碳(CCl4)处理暴露于109Cd的大鼠,并研究镉(Cd)在体内的分布。肝脏中的镉随着CCl4剂量的增加而显著降低。与之形成对比的是,血浆、肾脏和尿液中的镉显著增加。其他组织和粪便中的镉未观察到明显变化。这些现象也由其他肝毒素如半乳糖胺和乙硫氨酸以及长期给予镉所引起。在血浆镉显著增加的每种情况下,血浆谷氨酸草酰乙酸转氨酶(GOT)、谷氨酸丙酮酸转氨酶(GPT)和乳酸脱氢酶(LDH)水平同时升高,并且观察到血浆中镉浓度与每种酶活性之间存在显著的正相关。CCl4处理大鼠肝脏上清液中的镉大多与MT部分结合,在肾脏、血浆或尿液中,镉也以MT的形式存在。这些结果表明,在某些类型的肝脏疾病中,肝脏MT可以与肝脏酶以相同的方式释放到血液中,并转运至肾脏和尿液。

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引用本文的文献

1
Cadmium Complexed with β2-Microglubulin, Albumin and Lipocalin-2 rather than Metallothionein Cause Megalin:Cubilin Dependent Toxicity of the Renal Proximal Tubule.镉与β2-微球蛋白、白蛋白和脂联素-2形成复合物,而不是金属硫蛋白,导致巨球蛋白:内收蛋白依赖性肾近端小管毒性。
Int J Mol Sci. 2019 May 14;20(10):2379. doi: 10.3390/ijms20102379.
2
Acute kidney injury following acute liver failure: potential role of systemic cadmium mobilization?急性肝衰竭后急性肾损伤:全身性镉动员的潜在作用?
Intensive Care Med. 2012 Mar;38(3):467-73. doi: 10.1007/s00134-011-2449-0. Epub 2012 Jan 12.
3
Studies of cadmium uptake and metabolism by the kidney.
肾脏对镉的摄取与代谢研究。
Environ Health Perspect. 1984 Mar;54:21-30. doi: 10.1289/ehp.845421.