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金属硫蛋白(MT)是一种低分子量,富含半胱氨酸可结合重金属的蛋白质。从微生物到脊椎动物由Cd、Zn、Cu、Ag、激素及各种应急诱导产生金属硫蛋白。金属硫蛋白主要参与重金属解毒及氧化损伤解毒,储存金属,调节Zn及Cu的代谢,清除自由基。金属硫蛋白基因的表达调控是在转录水平上进行的,通过与金属,糖皮质激素及血反应元素顺式作用,及与DNA-结合蛋白,金属调节蛋白的反式作用达到调节的作用。众所周知,MT与一些疾病的发病过程密切相关。科学研究广泛地探索了心脏MT的抗氧化功能。最近采用心脏定位的MT-表达过量的转基因小鼠模型研究结果强力支持MT的这一生理作用。在急性及慢性刺激下如用阿霉素处理、局部缺血-再灌注损伤、食物中铜的限制,MT-表达过量的转基因小鼠心脏显示了对损伤的显著抗性。实验结果表明MT调节免疫系统,但MT的主要功能还不清楚。
Metallothionein (MT) is a low-molecular-weight, cysteine-rich protein that binds heavy metals. From microorganisms to vertebrates, metallothioneins are produced by Cd, Zn, Cu, Ag, hormones and various emergencies. Metallothionein is mainly involved in detoxification of heavy metals and oxidative damage, stores metals, regulates the metabolism of Zn and Cu, and scavenges free radicals. Metallothionein gene expression regulation is at the transcriptional level, through the metal, glucocorticoid and blood reaction elements cis-acting, and DNA-binding protein, metalloprotein trans-regulatory role. As we all know, MT is closely related to the pathogenesis of some diseases. Scientific research has extensively explored the anti-oxidant function of cardiac MT. Recent findings using cardiac localization of MT-overexpressing transgenic mouse models strongly support this physiological role of MT. Transgenic mouse hearts with MT-overexpressed expression showed significant resistance to injury under acute and chronic stimuli such as treatment with doxorubicin, ischemia-reperfusion injury, copper restriction in food, and MT-over-expression. The experimental results show that MT regulate the immune system, but the main function of MT is not clear.