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本文引用的文献

1
Activation of apoptosis signal-regulating kinase 1 is a key factor in paraquat-induced cell death: modulation by the Nrf2/Trx axis.凋亡信号调节激酶 1 的激活是百草枯诱导细胞死亡的关键因素:Nrf2/Trx 轴的调节。
Free Radic Biol Med. 2010 May 15;48(10):1370-81. doi: 10.1016/j.freeradbiomed.2010.02.024. Epub 2010 Mar 2.
2
Paraquat and Parkinson's disease.百草枯与帕金森病。
Cell Death Differ. 2010 Jul;17(7):1115-25. doi: 10.1038/cdd.2009.217. Epub 2010 Jan 22.
3
Effects of chronic low dose rotenone treatment on human microglial cells.慢性低剂量鱼藤酮处理对人小胶质细胞的影响。
Mol Neurodegener. 2009 Dec 31;4:55. doi: 10.1186/1750-1326-4-55.
4
Differential contribution of the mitochondrial respiratory chain complexes to reactive oxygen species production by redox cycling agents implicated in parkinsonism.涉及帕金森病的氧化还原循环试剂产生活性氧物种中,线粒体呼吸链复合物的差异贡献。
Toxicol Sci. 2009 Dec;112(2):427-34. doi: 10.1093/toxsci/kfp223. Epub 2009 Sep 18.
5
Paraquat activates the IRE1/ASK1/JNK cascade associated with apoptosis in human neuroblastoma SH-SY5Y cells.百草枯激活人神经母细胞瘤SH-SY5Y细胞中与凋亡相关的IRE1/ASK1/JNK级联反应。
Toxicol Lett. 2009 Dec 15;191(2-3):203-10. doi: 10.1016/j.toxlet.2009.08.024. Epub 2009 Sep 6.
6
Cyclo(His-Pro) up-regulates heme oxygenase 1 via activation of Nrf2-ARE signalling.环(组氨酸-脯氨酸)通过激活Nrf2-ARE信号通路上调血红素加氧酶1。
J Neurochem. 2009 Nov;111(4):956-66. doi: 10.1111/j.1471-4159.2009.06376.x. Epub 2009 Sep 7.
7
Effects of paraquat-induced oxidative stress on the neuronal plasma membrane Ca(2+)-ATPase.百草枯诱导的氧化应激对神经元质膜 Ca(2+)-ATP 酶的影响。
Free Radic Biol Med. 2009 Nov 15;47(10):1507-14. doi: 10.1016/j.freeradbiomed.2009.08.018. Epub 2009 Aug 26.
8
LRRK2 modulates vulnerability to mitochondrial dysfunction in Caenorhabditis elegans.亮氨酸重复激酶2(LRRK2)调节秀丽隐杆线虫对线粒体功能障碍的易感性。
J Neurosci. 2009 Jul 22;29(29):9210-8. doi: 10.1523/JNEUROSCI.2281-09.2009.
9
Dopamine transporter genetic variants and pesticides in Parkinson's disease.帕金森病中的多巴胺转运体基因变异与农药
Environ Health Perspect. 2009 Jun;117(6):964-9. doi: 10.1289/ehp.0800277. Epub 2009 Feb 22.
10
The role of NADPH oxidase 1-derived reactive oxygen species in paraquat-mediated dopaminergic cell death.烟酰胺腺嘌呤二核苷酸磷酸氧化酶 1 衍生的活性氧在百草枯介导的多巴胺能细胞死亡中的作用。
Antioxid Redox Signal. 2009 Sep;11(9):2105-18. doi: 10.1089/ARS.2009.2459.

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.

DOI:10.1016/j.cbi.2010.06.003
PMID:20542017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2942983/
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。