Hasegawa T, Mihara M, Okuno T, Nakamuro K, Sayato Y
Division of Environmental Health, Faculty of Pharmaceutical Sciences, Setsunan University, Osaka, Japan.
Arch Toxicol. 1995;69(5):312-7. doi: 10.1007/s002040050176.
The chemical form of a selenium-containing metabolite in the small intestine following a single oral administration of selenocystine was investigated with ICR male mice. Selenium content in the small intestine of animals treated with 50 mg/kg selenocystine significantly increased 15 min, 1 h and 6 h after treatment. In contrast, selenocystine significantly depressed the intestinal reduced glutathione (GSH) level at 1 h after administration. A significant negative correlation between the selenium level and the level of GSH in the small intestine was observed (r = -0.83, p < 0.001). Analysis of the intestinal metabolite of selenocystine showed that selenium-containing metabolites elute in two fractions from a Sephadex G-25 column: the low-molecular fraction (peak I) contained the selenocystine, while the high-molecular fraction (peak II) contained selenocysteine-containing metabolite. An in vitro experiment was performed to gain insight into the mechanism for selenocysteine-containing metabolite production in the intestinal cytosol. When selenocystine or selenocysteine reacted with excess GSH in the presence of intestinal homogenate, the peak II fraction which involved the selenocysteine-containing metabolite was recognized in the Sephadex G-25 chromatogram. From an examination of the distribution of the selenocysteine-containing metabolite, it was recognized that this metabolite exists in plasma and liver cytosol of mice after oral administration of selenocystine. These results suggested that the mice treated with selenocystine produce selenocysteine-containing metabolite by reaction of selenocystine with excess GSH in the small intestine, and the metabolite is then transported to the liver through blood plasma.
利用ICR雄性小鼠研究了单次口服硒代胱氨酸后小肠中含硒代谢物的化学形式。用50mg/kg硒代胱氨酸处理的动物，小肠中的硒含量在处理后15分钟、1小时和6小时显著增加。相比之下，硒代胱氨酸在给药后1小时显著降低了肠道还原型谷胱甘肽（GSH）水平。观察到小肠中硒水平与GSH水平之间存在显著的负相关（r = -0.83，p < 0.001）。对硒代胱氨酸的肠道代谢物分析表明，含硒代谢物从Sephadex G-25柱中以两个馏分洗脱：低分子馏分（峰I）含有硒代胱氨酸，而高分子馏分（峰II）含有含硒代半胱氨酸的代谢物。进行了一项体外实验，以深入了解肠道细胞质中含硒代半胱氨酸代谢物的产生机制。当硒代胱氨酸或硒代半胱氨酸在肠道匀浆存在下与过量的GSH反应时，在Sephadex G-25色谱图中识别出涉及含硒代半胱氨酸代谢物的峰II馏分。通过检查含硒代半胱氨酸代谢物的分布，发现口服硒代胱氨酸后该代谢物存在于小鼠的血浆和肝脏细胞质中。这些结果表明，用硒代胱氨酸处理的小鼠通过硒代胱氨酸与小肠中过量的GSH反应产生含硒代半胱氨酸的代谢物，然后该代谢物通过血浆转运到肝脏。
