Mammalian zinc homeostasis: requirement for RNA and metallothionein synthesis.
Mammalian zinc homeostasis: requirement for RNA and metallothionein synthesis.
复制标题
哺乳动物锌稳态：RNA 和金属硫蛋白合成的需要。
DOI：
10.1016/0006-291x(75)90822-0
复制
发表时间：
1975
影响因子：
3.1
通讯作者：
Robert J. Cousins
中科院分区：
文献类型：
--
作者：
Mark P. Richards;Robert J. Cousins
采用肠道外给药锌负荷作为模型，研究大鼠体内锌稳态。血清锌随锌负荷的增加先升高后降低。这一下降伴随着肝细胞胞浆锌摄取和金属硫蛋白合成的增强。放线菌素D管理抑制锌摄取到肝细胞质和金属硫蛋白的合成。mRNA和金属硫蛋白的合成似乎是必要的肝锌摄取。锌负荷大鼠的肠道65 Zn吸收减少，但在锌负荷前接受放线菌素D治疗的大鼠中，肠道65 Zn吸收接近正常。吸收与血清锌含量无关，但与粘膜金属硫蛋白合成呈负相关，与锌螯合物直接相关。一个整体的稳态机制，提出了金属硫蛋白的合成控制在转录水平的身体锌状态。在肝脏中，金属硫蛋白合成在肝细胞中锌的摄取和储存中起作用。在肠粘膜细胞中，这种蛋白质与参与锌吸收的正常配体竞争，从而调节可转移到血浆的锌量。
A parenterally administered zinc load was used as a model to investigate zinc homeostasis in rats. Serum zinc increased markedly then decreased following the zinc load. The decrease was concomitant with enhanced zinc uptake into hepatocyte cytosol and metallothionein synthesis. Actinomycin D administration inhibited zinc uptake into liver cytosol and metallothionein synthesis. Both mRNA and metallothionein synthesis appear to be necessary for hepatic zinc uptake. Intestinal65Zn absorption was decreased in zinc loaded rats but was near normal in rats treated with actinomycin D prior to the zinc load. Absorption was not correlated with the serum zinc content but was inversely related to mucosal metallothionein synthesis and directly related to a zinc chelate complex. An overall homeostatic mechanism is proposed where metallothionein synthesis is controlled at the transcriptional level by body zinc status. In the liver, metallothionein synthesis functions in uptake and storage of zinc in hepatocytes. In the intestinal mucosal cells this protein competes with the normal ligand involved in zinc absorption and thus regulates the amount of zinc available for transfer to the plasma.