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线粒体功能障碍是否在锰毒性中起作用?

Could mitochondrial dysfunction play a role in manganese toxicity?

机构信息

Institute of Fundamental Sciences-Chemistry, Massey University, Private Bag 11222, Palmerston North, New Zealand.

出版信息

Environ Toxicol Pharmacol. 1999 Mar;7(1):49-57. doi: 10.1016/s1382-6689(98)00054-4.

DOI:10.1016/s1382-6689(98)00054-4
PMID:21781909
Abstract

Individuals suffering from manganese toxicity exhibit several symptoms, including mitochondrial dysfunction, which are similar to those frequently observed in cases of Parkinson's disease. We review the literature concerning manganese toxicity and mitochondrial function, and propose a simple conceptual model of the aetiology of manganese toxicity which involves an interaction between inhibition of mitochondrial energy transduction, generation of free radicals and mutations of the mitochondrial genome. This conceptual model prompts a number of relatively simple experiments which would provide a test of the model.

摘要

患有锰中毒的个体表现出多种症状,包括线粒体功能障碍,这些症状与帕金森病患者中经常观察到的症状相似。我们回顾了锰中毒和线粒体功能的文献,并提出了一个简单的锰中毒病因学概念模型,该模型涉及线粒体能量转导抑制、自由基生成和线粒体基因组突变之间的相互作用。这个概念模型提示了一些相对简单的实验,这些实验将为该模型提供测试。

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Could mitochondrial dysfunction play a role in manganese toxicity?线粒体功能障碍是否在锰毒性中起作用?
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