Watanabe C, Ohba T, Nakahara H, Suzuki T
Department of Human Ecology, School of Health Sciences, Faculty of Medicine, University of Tokyo, Japan.
Toxicology. 1988 Oct;51(2-3):167-76. doi: 10.1016/0300-483x(88)90147-3.
The effects of co-administration of reduced glutathione (GSH) on the lethality of sodium selenite (SS) and on SS-induced hypothermia and hyperphagia were examined in adult male ICR mice. Tissue GSH levels after s.c. injection were also determined. In the plasma, GSH concentration was significantly elevated up to 2 h after injection of 2 mmol/kg of GSH. Little change was observed in liver, and erythrocyte levels, the lethality of SS was enhanced by a similar dose of GSH. This enhancement, however, was observed only when SS was injected during the period when plasma GSH was elevated. These results suggest that the interaction between GSH and SS in plasma was the major contributor to the enhancement of SS toxicity. Hypothermia induced by SS was also enhanced by a 60-fold dose of GSH but not by a 6-fold dose of GSH. With respect to hyperphagia, GSH suppressed the effect of SS, probably because of depressing effect of co-administration of SS an GSH.
在成年雄性ICR小鼠中，研究了联合给予还原型谷胱甘肽（GSH）对亚硒酸钠（SS）致死率以及SS诱导的体温过低和摄食过多的影响。还测定了皮下注射后组织中的GSH水平。在血浆中，注射2 mmol/kg GSH后2小时内，GSH浓度显著升高。肝脏和红细胞中的水平变化不大，相似剂量的GSH可增强SS的致死率。然而，这种增强仅在血浆GSH升高期间注射SS时才观察到。这些结果表明，血浆中GSH与SS之间的相互作用是SS毒性增强的主要原因。SS诱导的体温过低也可被60倍剂量的GSH增强，但6倍剂量的GSH则无此作用。关于摄食过多，GSH抑制了SS的作用，这可能是由于联合给予SS和GSH的抑制作用。
