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膳食甲基汞对幼年白鲸(Huso huso)大脑蛋白质组的修饰作用。

Proteome modifications of juvenile beluga (Huso huso) brain as an effect of dietary methylmercury.

机构信息

Department of Fisheries, Faculty of Marine Natural Resources, Khorramshahr University of Marine Science and Technology, Khorramshahr, Khouzestan, Iran.

Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran.

出版信息

Comp Biochem Physiol Part D Genomics Proteomics. 2009 Dec;4(4):243-248. doi: 10.1016/j.cbd.2009.01.002. Epub 2009 Jan 23.

DOI:10.1016/j.cbd.2009.01.002
PMID:20403756
Abstract

Methylmercury (MeHg) is the most toxic form of mercury which is bioaccumulated in the aquatic food chain. It has been shown that one of the main targets of MeHg toxicity is the brain, but there is little knowledge of the molecular mechanisms of its toxic effects. In this work we used a proteomics analysis to determine the changes in the brain proteome of juvenile beluga (Huso huso) exposed to dietary MeHg. The juvenile beluga were fed the diet containing 0.8 ppm MeHg for 70 days. Proteins of the brain tissue were analyzed using two-dimensional electrophoresis and MALDI-TOF/TOF mass spectrometry. We found eight proteins with significant altered expression level in the fish brain exposed to MeHg. These proteins are involved in different cell functions including cell metabolism, protein folding, cell division, and signal transduction. Our results support the idea that MeHg exerts its toxicity through oxidative stress induction and apoptotic effects. They also suggest that chronic MeHg exposure would induce an important metabolic deficiency in the brain. These findings provide basic information to understand possible mechanisms of MeHg toxicity in aquatic ecosystems.

摘要

甲基汞(MeHg)是汞的毒性最强的形式,在水生食物链中生物累积。已经表明,MeHg 毒性的主要靶标之一是大脑,但对其毒性作用的分子机制知之甚少。在这项工作中,我们使用蛋白质组学分析来确定暴露于膳食 MeHg 的幼年白鲸(Huso huso)大脑蛋白质组的变化。幼年白鲸喂食含有 0.8ppm MeHg 的饮食 70 天。使用二维电泳和 MALDI-TOF/TOF 质谱分析法分析脑组织中的蛋白质。我们发现,暴露于 MeHg 的鱼脑中有八种蛋白质的表达水平有显著变化。这些蛋白质参与不同的细胞功能,包括细胞代谢、蛋白质折叠、细胞分裂和信号转导。我们的研究结果支持 MeHg 通过诱导氧化应激和凋亡作用发挥其毒性的观点。它们还表明,慢性 MeHg 暴露会导致大脑发生重要的代谢缺陷。这些发现为理解水生生态系统中 MeHg 毒性的可能机制提供了基础信息。

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