Pezerović D, Narancsik P, Gamulin S
Arch Toxicol. 1981 Sep;48(2-3):167-72. doi: 10.1007/BF00310485.
Polyribosome sedimentation pattern and their in vitro protein synthetic ability were investigated in kidneys of mice treated with a single injection of HgCl2. Mercury bichloride, after 1 h, evokes polyribosome disaggregation, the extent of which is logarithmically correlated with the dose in the range of 2.5-20 micromoles/kg. With the dose of 2.5 micromoles/kg the effect occurs in 1 h, it is maximal between 1 h and 3 h. After 6 h polyribosomes are reaggregated. Cycloheximide pretreatment does not prevent the HgCl2 induced disaggregation of kidney polyribosomes. The cell-free system derived from kidneys of HgCl2 treated mice (10 micromoles/kg, 1 h) has a decreased protein synthetic ability. Both, in livers of mice treated with 20 micromoles/kg HgCl2 and in isolated rat's reticulocytes incubated with 20 micro M HgCl2 during 1 h there were no apparent changes in the polyribosome sedimentation patterns.
研究了单次注射氯化汞处理的小鼠肾脏中的多核糖体沉降模式及其体外蛋白质合成能力。氯化汞在1小时后引起多核糖体解聚，在2.5 - 20微摩尔/千克范围内，解聚程度与剂量呈对数相关。剂量为2.5微摩尔/千克时，1小时出现效应，在1小时至3小时之间效应最大。6小时后多核糖体重新聚集。环己酰亚胺预处理不能阻止氯化汞诱导的肾脏多核糖体解聚。来自氯化汞处理小鼠（10微摩尔/千克，1小时）肾脏的无细胞系统蛋白质合成能力下降。在用20微摩尔/千克氯化汞处理的小鼠肝脏以及在1小时内用20微摩尔氯化汞孵育的分离大鼠网织红细胞中，多核糖体沉降模式均无明显变化。
