百草枯和铁暴露作为帕金森病中可能的协同环境风险因素。 - Suppr

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超能文献

Paraquat and iron exposure as possible synergistic environmental risk factors in Parkinson's disease.

作者信息

Andersen Julie K

机构信息

Buck Institute for Age Research, 8001 Redwood Blvd., Novato, CA 94945, USA.

出版信息

Neurotox Res. 2003;5(5):307-13. doi: 10.1007/BF03033150.

DOI:10.1007/BF03033150

PMID:14715449

Abstract

摘要

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Paraquat and iron exposure as possible synergistic environmental risk factors in Parkinson's disease.百草枯和铁暴露作为帕金森病中可能的协同环境风险因素。

Neurotox Res. 2003;5(5):307-13. doi: 10.1007/BF03033150.

Environmental risk factors and Parkinson's disease: selective degeneration of nigral dopaminergic neurons caused by the herbicide paraquat.环境风险因素与帕金森病：除草剂百草枯导致黑质多巴胺能神经元的选择性退化

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Rotenone and paraquat linked to Parkinson's disease: human exposure study supports years of animal studies.鱼藤酮和百草枯与帕金森病有关：人体暴露研究证实了多年的动物研究结果。

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Combined exposure to agriculture pesticides, paraquat and maneb, induces alterations in the N/OFQ-NOPr and PDYN/KOPr systems in rats: Relevance to sporadic Parkinson's disease.联合暴露于农业杀虫剂百草枯和代森锰，会引起大鼠中孤啡肽 - 孤啡肽受体系统及强啡肽 - κ阿片受体系统的改变：与散发性帕金森病的相关性

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A slowly developing dysfunction of dopaminergic nigrostriatal neurons induced by long-term paraquat administration in rats: an animal model of preclinical stages of Parkinson's disease?长期给大鼠施用百草枯诱导的多巴胺能黑质纹状体神经元缓慢发展的功能障碍：帕金森病临床前期的动物模型？

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Epidemiology. Paths from pesticides to Parkinson's.流行病学。从农药到帕金森病的路径。

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Pooled analysis of iron-related genes in Parkinson's disease: association with transferrin.帕金森病中铁相关基因的荟萃分析：与转铁蛋白的关联。

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Effects of age, gender, and gonadectomy on neurochemistry and behavior in animal models of Parkinson's disease.年龄、性别和性腺切除术对帕金森病动物模型神经化学及行为的影响。

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本文引用的文献

Genetic or pharmacological iron chelation prevents MPTP-induced neurotoxicity in vivo: a novel therapy for Parkinson's disease.基因或药物性铁螯合可预防体内MPTP诱导的神经毒性：一种治疗帕金森病的新疗法。

Neuron. 2003 Mar 27;37(6):899-909. doi: 10.1016/s0896-6273(03)00126-0.

Effects of L-dopa and other amino acids against paraquat-induced nigrostriatal degeneration.

J Neurochem. 2003 Apr;85(1):82-6. doi: 10.1046/j.1471-4159.2003.01621.x.

Neurobiol Dis. 2002 Jul;10(2):119-27. doi: 10.1006/nbdi.2002.0507.

Human alpha-synuclein over-expression increases intracellular reactive oxygen species levels and susceptibility to dopamine.人类α-突触核蛋白的过度表达会增加细胞内活性氧水平以及对多巴胺的敏感性。

Neurosci Lett. 2002 Mar 8;320(3):146-50. doi: 10.1016/s0304-3940(02)00016-2.

Glutathione decreases in dopaminergic PC12 cells interfere with the ubiquitin protein degradation pathway: relevance for Parkinson's disease?多巴胺能PC12细胞中谷胱甘肽的减少干扰泛素蛋白降解途径：与帕金森病的相关性？

J Neurochem. 2002 Feb;80(4):555-61. doi: 10.1046/j.0022-3042.2001.00009.x.

alpha-Synuclein protects against oxidative stress via inactivation of the c-Jun N-terminal kinase stress-signaling pathway in neuronal cells.α-突触核蛋白通过使神经元细胞中的c-Jun氨基末端激酶应激信号通路失活来抵御氧化应激。

J Biol Chem. 2002 Mar 29;277(13):11465-72. doi: 10.1074/jbc.M111428200. Epub 2002 Jan 14.

The herbicide paraquat causes up-regulation and aggregation of alpha-synuclein in mice: paraquat and alpha-synuclein.除草剂百草枯可导致小鼠体内α-突触核蛋白上调和聚集：百草枯与α-突触核蛋白。

J Biol Chem. 2002 Jan 18;277(3):1641-4. doi: 10.1074/jbc.C100560200. Epub 2001 Nov 13.

Metal-triggered structural transformations, aggregation, and fibrillation of human alpha-synuclein. A possible molecular NK between Parkinson's disease and heavy metal exposure.金属引发的人α-突触核蛋白的结构转变、聚集和纤维化。帕金森病与重金属暴露之间可能的分子联系。

J Biol Chem. 2001 Nov 23;276(47):44284-96. doi: 10.1074/jbc.M105343200. Epub 2001 Sep 11.

Pesticides directly accelerate the rate of alpha-synuclein fibril formation: a possible factor in Parkinson's disease.农药直接加速α-突触核蛋白原纤维的形成：帕金森病的一个可能因素。

FEBS Lett. 2001 Jul 6;500(3):105-8. doi: 10.1016/s0014-5793(01)02597-2.

Carrier-mediated processes in blood--brain barrier penetration and neural uptake of paraquat.血液-脑屏障穿透及百草枯神经摄取中的载体介导过程。

Brain Res. 2001 Jul 6;906(1-2):135-42. doi: 10.1016/s0006-8993(01)02577-x.

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