Cheung M K, Verity M A
Exp Mol Pathol. 1983 Apr;38(2):230-42. doi: 10.1016/0014-4800(83)90088-6.
Perturbation of brain protein synthesis by methyl mercury chloride (MeHg) was compared in vivo and in vitro. MeHg-stimulated and/or inhibited brain cell-free protein synthesis following in vivo or in vitro administration. Although pretreatment with GSH protected the postmitochondrial supernatant (PMS) from the in vitro inhibition, direct addition of -SH compounds did not reverse the in vivo or in vitro perturbations in synthesis induced by MeHg. Inhibition of synthesis induced by both in vivo and in vitro methyl mercury administration resulted in inactivation of component(s) in brain pH 5 enzymes. Stimulation of amino acid incorporation following in vivo administration of MeHg was apparently associated with the ribosome fraction, but in vitro preincubation of PMS with MeHg produced stimulation associated with the pH 5 enzyme fraction. A model of MeHg neurotoxicity was proposed providing a common molecular locus of interaction in vivo and in vitro.
在体内和体外比较了氯化甲基汞(MeHg)对脑蛋白质合成的干扰。体内或体外给予MeHg后,其刺激和/或抑制了无细胞体系中的脑细胞蛋白质合成。尽管用谷胱甘肽(GSH)预处理可保护线粒体后上清液(PMS)免受体外抑制,但直接添加巯基化合物并不能逆转MeHg诱导的体内或体外合成干扰。体内和体外给予甲基汞诱导的合成抑制导致脑pH 5酶中的组分失活。体内给予MeHg后氨基酸掺入的刺激显然与核糖体部分有关,但PMS与MeHg的体外预孵育产生的刺激与pH 5酶部分有关。提出了一个MeHg神经毒性模型,该模型提供了体内和体外相互作用的共同分子位点。