Long M, Zhao J, Wang S
Department of Preventive Medicine, Guiyang Medical College, Guizhou.
Zhonghua Yu Fang Yi Xue Za Zhi. 1998 Mar;32(2):73-5.
To understand the possible role of trace elements in renal damage caused by cadmium poisoning and its mechanism.
An experimental animal model with renal damage caused by cadmium poisoning was prepared, and trace elements contents in subcellular components in renal cells, lipid peroxidation reaction, renal function and its ultrastructural changes were determined.
Uptake of cadmium could cause transfer of copper, zinc and manganese mainly distributed in the mitochondrion to cell nuclei and cytoplasm, and content of selenium and activity of glutathione-peroxidase (GSH-px) in cytosol declined and content of propandiolal increased.
It suggests that changes in trace elements contents, especially in selenium content, during renal damage caused by cadmium poisoning, could correlate with the increase of lipid peroxidation, and abnormal subcellular distribution of trace elements was one of the important roles in renal damage caused by cadmium poisoning.
了解微量元素在镉中毒致肾损害中的可能作用及其机制。
制备镉中毒致肾损害的实验动物模型,检测肾细胞亚细胞成分中的微量元素含量、脂质过氧化反应、肾功能及其超微结构变化。
镉的摄入可使主要分布于线粒体的铜、锌、锰转移至细胞核和细胞质,胞质中硒含量及谷胱甘肽过氧化物酶(GSH-px)活性下降,丙二醛含量增加。
提示镉中毒致肾损害过程中微量元素含量的变化,尤其是硒含量的变化,可能与脂质过氧化增加有关,微量元素的亚细胞分布异常是镉中毒致肾损害的重要作用之一。