Nishikido N, Satoh Y, Iwai I, Ishii M, Naganuma A, Imura N
Department of Public Health School of Pharmaceutical Sciences Kitasato University, Tokyo, Japan.
Toxicol Appl Pharmacol. 1988 Mar 15;92(3):497-9. doi: 10.1016/0041-008x(88)90189-5.
We have recently reported that maternal administration of methylmercury caused a striking increase in the selenium concentration in fetal liver accompanied by a decrease in selenium-dependent glutathione peroxidase (GSH-Px) activity. These changes resulted in the lowered bioavailability of selenium as far as the GSH-Px activity was concerned. The present study demonstrated that maternal administration of methylmercury caused a specific alteration of the form of selenium in fetal liver. Sephadex G-200 gel filtration of liver cytosols revealed an additional major peak of selenium in the fetal livers of mice treated with methylmercury. This peak was not present in the liver, kidney, or placenta of mothers treated with methylmercury.
我们最近报道,母体给予甲基汞会导致胎肝中硒浓度显著升高,同时硒依赖性谷胱甘肽过氧化物酶(GSH-Px)活性降低。就GSH-Px活性而言,这些变化导致硒的生物利用度降低。本研究表明,母体给予甲基汞会导致胎肝中硒的形态发生特异性改变。对肝脏胞质溶胶进行葡聚糖凝胶G-200过滤显示,用甲基汞处理的小鼠胎肝中出现了一个额外的主要硒峰。在用甲基汞处理的母体的肝脏、肾脏或胎盘中不存在这个峰。