Masukawa T, Nishimura T, Kito H, Iwata H
J Pharmacobiodyn. 1983 Dec;6(12):950-3. doi: 10.1248/bpb1978.6.950.
This study was undertaken to examine a possible role of bis(methylmercuric) selenide(BMS) in selenite-induced redistribution of methylmercury in rats. Pretreatment of diethylmaleate(DEM), which depletes tissue reduced glutathione(GSH), completely suppressed the significant increase of BMS produced by selenite injection in the blood of methylmercury-treated rats. Its inhibitory effect was also observed in the kidney and brain. Under the same conditions, the characteristic accumulation in the brain and testis of total mercury induced by selenite was markedly inhibited by DEM pretreatment. Total mercury in these tissues was not altered by DEM alone and BMS in the blood existed in the erythrocytes, but not in the plasma. Thus, it seems likely that the suppressed formation of BMS in the erythrocytes mainly leads to the decreased accumulation of total mercury in the brain and testis.
本研究旨在探讨双(甲基汞)硒化物(BMS)在亚硒酸盐诱导的甲基汞在大鼠体内重新分布中可能发挥的作用。马来酸二乙酯(DEM)可耗尽组织中的还原型谷胱甘肽(GSH),对经甲基汞处理的大鼠进行DEM预处理后,完全抑制了亚硒酸盐注射导致的血液中BMS显著增加。在肾脏和大脑中也观察到了其抑制作用。在相同条件下,DEM预处理显著抑制了亚硒酸盐诱导的大脑和睾丸中总汞的特征性蓄积。单独使用DEM不会改变这些组织中的总汞含量,血液中的BMS存在于红细胞中,而非血浆中。因此,红细胞中BMS生成受抑制似乎主要导致大脑和睾丸中总汞蓄积减少。