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农药诱导神经毒性的分子机制:与帕金森病的关系。

Molecular mechanisms of pesticide-induced neurotoxicity: Relevance to Parkinson's disease.

机构信息

Redox Biology Center, University of Nebraska-Lincoln, 68583, United States.

出版信息

Chem Biol Interact. 2010 Nov 5;188(2):289-300. doi: 10.1016/j.cbi.2010.06.003. Epub 2010 Jun 11.

Abstract

Pesticides are widely used in agricultural and other settings, resulting in continued human exposure. Pesticide toxicity has been clearly demonstrated to alter a variety of neurological functions. Particularly, there is strong evidence suggesting that pesticide exposure predisposes to neurodegenerative diseases. Epidemiological data have suggested a relationship between pesticide exposure and brain neurodegeneration. However, an increasing debate has aroused regarding this issue. Paraquat is a highly toxic quaternary nitrogen herbicide which has been largely studied as a model for Parkinson's disease providing valuable insight into the molecular mechanisms involved in the toxic effects of pesticides and their role in the progression of neurodegenerative diseases. In this work, we review the molecular mechanisms involved in the neurotoxic action of pesticides, with emphasis on the mechanisms associated with the induction of neuronal cell death by paraquat as a model for Parkinsonian neurodegeneration.

摘要

农药在农业和其他领域被广泛使用,导致人类持续暴露其中。农药毒性已被明确证实会改变多种神经功能。特别是,有强有力的证据表明,农药暴露会导致神经退行性疾病。流行病学数据表明,农药暴露与脑神经退行性变之间存在关联。然而,关于这个问题的争论越来越多。百草枯是一种剧毒的季铵氮除草剂,它作为帕金森病的模型被广泛研究,为了解农药的毒性作用及其在神经退行性疾病进展中的作用的分子机制提供了有价值的见解。在这项工作中,我们综述了农药神经毒性作用涉及的分子机制,重点介绍了百草枯诱导神经元细胞死亡的机制,将其作为帕金森神经退行性变的模型。

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