Turnover of metallothioneins in rat liver.
Turnover of metallothioneins in rat liver.
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大鼠肝脏中金属硫蛋白的周转。
DOI：
10.1042/bj1740327
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发表时间：
1978
期刊：
影响因子：
--
通讯作者：
I. Bernstein
中科院分区：
文献类型：
--
作者：
R. D. Andersen;W. Winter;J. Maher;I. Bernstein
从Cd ~（2+）处理的大鼠肝脏中分离出两种可区分的金属硫蛋白，其巯基/金属比为3：1，在这些蛋白质中的每一种中，总金属含量为3.6个Cd ~（2+）原子+2.4个Zn ~（2+）原子/分子和4.2个Cd ~（2+）原子+2.8个Zn ~（2+）原子/分子以及各自的载脂蛋白mol. wt.。5844和6251。与1小时脉冲标记的[3 H]半胱氨酸，单次注射后的ZnCl 2或CdCl 2的研究表明，这些金属刺激放射性同位素掺入金属硫蛋白超过对照值分别为10和15倍。这种刺激是最大的，在4小时后，一个单一的氯化镉注射，并降低到控制值的16小时，这表明无论是翻译事件响应游离细胞内镉或短寿命的mRNA正在产生或稳定的金属处理。在大鼠慢性暴露于氯化镉，金属硫蛋白增加到0.2%的肝湿重从对照值2- 4 μ mol/kg的肝脏，与最大的积累速度为2- 3 μ mol/h每公斤的肝脏。在对照组动物中，这些蛋白质的周转率为0.3- 0.6 mumoles/h/kg肝脏，通过与金属硫蛋白不可逆结合的~（203）Hg ~（2+）的消失率测量。预处理与氯化镉完全停止快速203汞营业额在未经处理的动物。与CdCl 2不同，ZnCl 2处理10 h后，金属硫蛋白浓度增加至新的稳态池，11 mumole/kg肝脏。通过暴露于ZnCl 2在体内锌硫蛋白池的增加被确定为主要是由于金属硫蛋白生物合成的刺激。
Two electrophoretically distinguishable metallothioneins were isolated from the livers of Cd2+-treated rats and had thiol group/metal ratios of 3:1, a total metal content, in each of these proteins, of 3.6 atoms of Cd2+ + 2.4 atoms of Zn2+/molecule and 4.2 atoms of Cd2+ + 2.8 atoms of Zn2+/molecule and respective apoprotein mol.wts. of 5844 and 6251. Studies with 1 h pulse labels of [3H]cysteine, given after a single injection of ZnCl2 or CdCl2, showed that these metals stimulated radioactive isotope incorporation into the metallothioneins over the control value by 10- and 15-fold respectively. This stimulation was maximal at 4 h after a single CdCl2 injection and decreased to control values by 16 h, suggesting that either a translational event is responding to free intracellular Cd2+ or a short-lived mRNA is being produced or stabilized in response to the metal treatment. In rats chronically exposed to CdCl2, the metallothioneins increased to 0.2% of the liver wet weight from a control value of 2--4 mumol/kg of liver, with a maximum rate of accumulation of 2--3 mumol/h per kg of liver. The turnover of these proteins in control animals was 0.3--0.6 mumoles/h per kg of liver, measured by the rate of disappearance of 203Hg2+, which binds irreversibly to the metallothioneins. Pretreatment with CdCl2 completely stopped the rapid 203Hg turnover observed in untreated animals. Unlike CdCl2, treatment with ZnCl2 increased the concentration of metallothioneins to a new steady-state pool, 11 mumole/kg of liver, after 10 h. The increase in the zinc-thionein pool by exposure to ZnCl2 in vivo was determined to be primarily due to a stimulation of metallothionein biosynthesis.