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百草枯令人费解的悖论:基于宿主易感性及假定的神经退行性影响的情况

The perplexing paradox of paraquat: the case for host-based susceptibility and postulated neurodegenerative effects.

作者信息

Jones Byron C, Huang Xuemei, Mailman Richard B, Lu Lu, Williams Robert W

机构信息

Department of Biobehavioral Health, The Pennsylvania State University, University Park, PA, USA; Department of Pharmacology, The Pennsylvania State University-Milton S. Hershey Medical Center, Hershey, PA, USA.

出版信息

J Biochem Mol Toxicol. 2014 May;28(5):191-7. doi: 10.1002/jbt.21552. Epub 2014 Mar 5.

DOI:10.1002/jbt.21552
PMID:24599642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4677573/
Abstract

Paraquat is an herbicide used extensively in agriculture and has also been proposed to be a risk factor for Parkinson's disease. To date, experimental, clinical, and epidemiological data on paraquat neurotoxicity have been equivocal. In this short review, we discuss some technical and biological mechanisms that contribute to inconsistencies regarding paraquat neurotoxicity. We hypothesize that individual genetic variations in susceptibility generate major differences in neurotoxic risk and functional outcome. Identifying these heritable sources of variation in host susceptibility, and their role in complex gene-environment interactions, is crucial to identify risk biomarkers and to devise better prevention and treatment for those exposed to paraquat and other potential neurotoxicants.

摘要

百草枯是一种在农业中广泛使用的除草剂,也被认为是帕金森病的一个风险因素。迄今为止,关于百草枯神经毒性的实验、临床和流行病学数据一直存在争议。在这篇简短的综述中,我们讨论了一些导致百草枯神经毒性研究结果不一致的技术和生物学机制。我们假设个体易感性的基因变异会导致神经毒性风险和功能结果产生重大差异。识别宿主易感性中这些可遗传的变异来源及其在复杂基因-环境相互作用中的作用,对于识别风险生物标志物以及为接触百草枯和其他潜在神经毒物的人群设计更好的预防和治疗方法至关重要。

相似文献

1
The perplexing paradox of paraquat: the case for host-based susceptibility and postulated neurodegenerative effects.百草枯令人费解的悖论:基于宿主易感性及假定的神经退行性影响的情况
J Biochem Mol Toxicol. 2014 May;28(5):191-7. doi: 10.1002/jbt.21552. Epub 2014 Mar 5.
2
Letter to the editor. Re: The perplexing paradox of paraquat: the case for host-based susceptibility and postulated neurodegenerative effects.致编辑的信。主题:百草枯令人困惑的悖论:基于宿主易感性及假定的神经退行性变效应的情况
J Biochem Mol Toxicol. 2014 Jul;28(7):289-90. doi: 10.1002/jbt.21591_1.
3
Response.回应。
J Biochem Mol Toxicol. 2014 Jul;28(7):291. doi: 10.1002/jbt.21591_2.
4
Genetic-based, differential susceptibility to paraquat neurotoxicity in mice.基于遗传的对百草枯神经毒性的差异易感性在小鼠中。
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HFE Genotype Restricts the Response to Paraquat in a Mouse Model of Neurotoxicity.HFE 基因型限制了神经毒性小鼠模型对百草枯的反应。
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Paraquat and maneb induced neurotoxicity.百草枯和代森锰诱导神经毒性。
Proc West Pharmacol Soc. 2007;50:31-42.
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Paraquat exposure induces Parkinsonism by altering lipid profile and evoking neuroinflammation in the midbrain.百草枯暴露通过改变脂质谱并引发中脑神经炎症引起帕金森病。
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Paraquat induces oxidative stress and neuronal cell death; neuroprotection by water-soluble Coenzyme Q10.百草枯诱导氧化应激和神经元细胞死亡;水溶性辅酶Q10的神经保护作用。
Toxicol Appl Pharmacol. 2004 Nov 15;201(1):21-31. doi: 10.1016/j.taap.2004.04.019.

引用本文的文献

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Paraquat Toxicogenetics: Strain-Related Reduction of Tyrosine Hydroxylase Staining in in Mice.百草枯毒理遗传学:小鼠中酪氨酸羟化酶染色的品系相关减少
Front Toxicol. 2021 Nov 11;3:722518. doi: 10.3389/ftox.2021.722518. eCollection 2021.
2
HFE H63D Limits Nigral Vulnerability to Paraquat in Agricultural Workers.载脂蛋白 H63D 限制农业工人中百草枯引起的黑质易损性。
Toxicol Sci. 2021 Apr 27;181(1):47-57. doi: 10.1093/toxsci/kfab020.
3
Pesticide use and incident Parkinson's disease in a cohort of farmers and their spouses.农药使用与农民及其配偶帕金森病发病风险的队列研究。
Environ Res. 2020 Dec;191:110186. doi: 10.1016/j.envres.2020.110186. Epub 2020 Sep 10.
4
Systems Genetics and Systems Biology Analysis of Paraquat Neurotoxicity in BXD Recombinant Inbred Mice.百草枯对BXD重组近交系小鼠神经毒性的系统遗传学和系统生物学分析
Toxicol Sci. 2020 Jul 1;176(1):137-146. doi: 10.1093/toxsci/kfaa050.
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Environmental neurotoxicant-induced dopaminergic neurodegeneration: a potential link to impaired neuroinflammatory mechanisms.环境神经毒性诱导的多巴胺能神经退行性变:与神经炎症机制受损的潜在关联。
Pharmacol Ther. 2019 May;197:61-82. doi: 10.1016/j.pharmthera.2019.01.001. Epub 2019 Jan 22.
6
Modification of Wnt signaling pathway on paraquat-induced inhibition of neural progenitor cell proliferation.百草枯诱导神经祖细胞增殖抑制中 Wnt 信号通路的修饰。
Food Chem Toxicol. 2018 Nov;121:311-325. doi: 10.1016/j.fct.2018.08.064. Epub 2018 Aug 30.
7
Assessment of the Effects of MPTP and Paraquat on Dopaminergic Neurons and Microglia in the Substantia Nigra Pars Compacta of C57BL/6 Mice.评估MPTP和百草枯对C57BL/6小鼠黑质致密部多巴胺能神经元和小胶质细胞的影响。
PLoS One. 2016 Oct 27;11(10):e0164094. doi: 10.1371/journal.pone.0164094. eCollection 2016.
8
Response to: Neurotoxicity of paraquat and paraquat-induced Parkinson's disease.回应:百草枯的神经毒性与百草枯诱发的帕金森病
Lab Invest. 2016 Sep;96(9):1030-4. doi: 10.1038/labinvest.2016.83.
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Parkinson's Disease: The Mitochondria-Iron Link.帕金森病:线粒体与铁的联系
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Synergistic stress exacerbation in hippocampal neurons: Evidence favoring the dual-hit hypothesis of neurodegeneration.海马神经元中的协同应激加剧:支持神经退行性变双重打击假说的证据。
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本文引用的文献

1
Microstructural changes in the substantia nigra of asymptomatic agricultural workers.无症状农业工人黑质的微观结构变化。
Neurotoxicol Teratol. 2014 Jan-Feb;41:60-4. doi: 10.1016/j.ntt.2013.12.001. Epub 2013 Dec 12.
2
Dietary fat intake, pesticide use, and Parkinson's disease.饮食中的脂肪摄入量、农药使用与帕金森病。
Parkinsonism Relat Disord. 2014 Jan;20(1):82-7. doi: 10.1016/j.parkreldis.2013.09.023. Epub 2013 Oct 1.
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Advances in the genetics of Parkinson disease.帕金森病遗传学研究进展。
Nat Rev Neurol. 2013 Aug;9(8):445-54. doi: 10.1038/nrneurol.2013.132. Epub 2013 Jul 16.
4
Response to Breckenridge et al. (2013).对布雷肯里奇等人(2013年)的回应。
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Systems analysis of genetic variation in MPTP neurotoxicity in mice.系统分析 MPTP 神经毒性在小鼠中的遗传变异。
Neurotoxicology. 2013 Jul;37:26-34. doi: 10.1016/j.neuro.2013.03.010. Epub 2013 Apr 1.
6
Pharmacokinetic, neurochemical, stereological and neuropathological studies on the potential effects of paraquat in the substantia nigra pars compacta and striatum of male C57BL/6J mice.百草枯对雄性 C57BL/6J 小鼠黑质致密部和纹状体潜在影响的药代动力学、神经化学、立体学和神经病理学研究。
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Age-related differences in iron content of subcortical nuclei observed in vivo: a meta-analysis.脑内皮质下核中铁含量的年龄相关性差异的体内观察:一项荟萃分析。
Neuroimage. 2013 Apr 15;70:113-21. doi: 10.1016/j.neuroimage.2012.12.040. Epub 2012 Dec 28.
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Parkinson's disease: evidence for environmental risk factors.帕金森病:环境风险因素的证据。
Mov Disord. 2013 Jan;28(1):8-13. doi: 10.1002/mds.25150. Epub 2012 Oct 24.
9
Iron metabolism: current facts and future directions.铁代谢:当前的事实和未来的方向。
Biochem Med (Zagreb). 2012;22(3):311-28. doi: 10.11613/bm.2012.034.
10
Meta-analysis of early nonmotor features and risk factors for Parkinson disease.帕金森病早期非运动特征及危险因素的荟萃分析。
Ann Neurol. 2012 Dec;72(6):893-901. doi: 10.1002/ana.23687. Epub 2012 Oct 15.