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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >The antioxidant properties of zinc and metallothionein.
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The antioxidant properties of zinc and metallothionein.

机译：锌和金属硫蛋白的抗氧化性能。

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Support for the hypothesis that metallothionein isoforms participate in intracellular defense against reactive oxygen and nitrogen species is derived from observations that substances causing oxidative stress, such as ethanol and iron, and agents involved in inflammatory processes, such as interleukin-1 and tumour necrosis factor alpha, induce the synthesis of metallothionein. Moreover, animals deficient in metallothionein isoforms exhibit greater susceptibility to oxidative stress; metallothionein genes are transcriptionally activated in cells and tissues during oxidative stress; and over expression of metallothionein reduces the sensitivity of cells and tissues to free radical-induced injury. In this study, we have shown that the i.c.v. administration of ZnSO4 increases the synthesis of metallothionein I mRNA and metallothionein II mRNA. In addition, the i.c.v. administration of ZnSO4 enhances the concentration of zinc and in direct proportion the synthesis of metallothionein mRNAs. Agents known to generate free radicals and to cause oxidative stress such as 6-hydroxydopamine, iron, hydrogen peroxide, and various alcohols lead to induction of metallothionein in the hippocampal neurons in primary culture and in Chang liver cells in culture. In view of the fact that zinc and 6-hydroxydopamine induce the level of brain metallothionein and its mRNAs and zinc and metallothionein concentrations vary in different regions of the brain, it is postulated that metallothionein may play a major role in nullifying the iron-mediated generation of free radicals and in protecting against oxidative stress in the brain.
机译：支持金属硫蛋白同工型参与细胞内对活性氧和氮物种防御的假说的支持来自以下观察：引起氧化应激的物质（例如乙醇和铁）以及参与炎症过程的物质（例如白介素-1和肿瘤坏死因子α） ，诱导金属硫蛋白的合成。而且，缺乏金属硫蛋白同工型的动物对氧化应激表现出更大的敏感性。金属硫蛋白基因在氧化应激期间在细胞和组织中被转录激活;金属硫蛋白的过度表达降低了细胞和组织对自由基诱导的损伤的敏感性。在这项研究中，我们证明了i.c.v. ZnSO 4的施用增加了金属硫蛋白I mRNA和金属硫蛋白II mRNA的合成。此外，i.c.v。施用ZnSO4可以提高锌的浓度，并直接成比例合成金属硫蛋白mRNA。已知会产生自由基并引起氧化应激的物质，例如6-羟基多巴胺，铁，过氧化氢和各种醇类，会在原代培养的海马神经元和培养的长肝细胞中诱导金属硫蛋白的诱导。鉴于锌和6-羟基多巴胺会诱导大脑中金属硫蛋白的水平及其mRNA以及锌和金属硫蛋白的浓度在大脑的不同区域发生变化这一事实，推测金属硫蛋白可能在使铁介导的生成无效的过程中起主要作用。自由基和防止大脑中的氧化应激。

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