Sato M, Sugano H, Takizawa Y
Arch Toxicol. 1981 Apr;47(2):125-33. doi: 10.1007/BF00332354.
The induction of metallothionein synthesis by administration of methylmercury chloride as studied. A repetitive sc dose of methylmercury chloride to rats in amounts of 10 mg/kg/day for 3 days produced profound hypozincemia and 3-fold increase in hepatic zinc bound to metallothionein by the initial 24 h. The incorporation of 35S-cysteine into hepatic metallothionein was about 4 times larger for rats treated with methylmercury, which was comparable with it for rats treated with cadmium, than for control rats. These results suggest the induction of de novo synthesis of metallothionein by administration of methylmercury, although methylmercury was found to be unable to bind to produced metallothionein both in vivo and in vitro. A stress produced by methylmercury administration appears to be involved in the induction of hepatic zinc-thionein by methylmercury, through its mechanism is not clear.
对通过给予氯化甲基汞来诱导金属硫蛋白合成进行了研究。以每天10毫克/千克的剂量对大鼠重复皮下注射氯化甲基汞,持续3天,在最初24小时内导致严重的低锌血症,并使肝脏中与金属硫蛋白结合的锌增加了3倍。对于用甲基汞处理的大鼠,35S-半胱氨酸掺入肝脏金属硫蛋白的量约为对照组大鼠的4倍,与用镉处理的大鼠相当。这些结果表明,给予甲基汞可诱导金属硫蛋白的从头合成,尽管发现甲基汞在体内和体外均无法与产生的金属硫蛋白结合。给予甲基汞产生的应激似乎参与了甲基汞对肝脏锌硫蛋白的诱导,但其机制尚不清楚。