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氯化汞导致小鼠脑锰超氧化物歧化酶蛋白的转录后水平升高。

Post-transcriptional elevation of mouse brain Mn-SOD protein by mercuric chloride.

作者信息

Kumagai Y, Mizukado S, Nagafune J, Shinyashiki M, Homma-Takeda S, Shimojo N

机构信息

Department of Environmental Medicine, Institute of Community Medicine, University of Tsukuba, Ibaraki, Japan.

出版信息

Brain Res. 1997 Sep 19;769(1):178-82. doi: 10.1016/s0006-8993(97)00846-9.

Abstract

Alterations in gene expression, protein content and enzyme activity of brain Mn-SOD following mercuric chloride (HgCl2) exposure were examined in ICR male mice. Subcutaneous administration of HgCl2 (1 mg Hg/kg) resulted in a significant increase (4-fold) in the brain Mn-SOD content at 6 h after injection while the total mercury concentration was about 0.11 microg/g of brain. The enhancement of Mn-SOD protein caused by HgCl2 was completely abolished by pretreatment with dexamethasone (3 mg/kg) 1 h prior to HgCl2 administration, suggesting involvement of inflammation in inorganic mercury-induced increase in the antioxidant enzyme. This increase in level of Mn-SOD content coincided with a substantial rise in the enzyme activity; however, Northern blot analysis revealed that the induction of protein level was not due to that of its gene expression. The results of the present study indicate that mouse brain Mn-SOD appears to undergo post-translational modification by the environmental toxic metal, and induction of the antioxidant enzyme could be of an initial response to the metal-induced oxidative stress.

摘要

在ICR雄性小鼠中检测了氯化汞(HgCl2)暴露后脑锰超氧化物歧化酶(Mn-SOD)的基因表达、蛋白质含量和酶活性变化。皮下注射HgCl2(1毫克汞/千克)导致注射后6小时脑Mn-SOD含量显著增加(4倍),而脑内总汞浓度约为0.11微克/克。在HgCl2给药前1小时用地塞米松(3毫克/千克)预处理可完全消除HgCl2引起的Mn-SOD蛋白增强,这表明炎症参与了无机汞诱导的抗氧化酶增加。Mn-SOD含量水平的这种增加与酶活性的大幅上升相一致;然而,Northern印迹分析表明,蛋白质水平的诱导并非由于其基因表达。本研究结果表明,小鼠脑Mn-SOD似乎受到环境有毒金属的翻译后修饰,抗氧化酶的诱导可能是对金属诱导的氧化应激的初始反应。

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