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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.
2
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
Neurobiol Dis. 2002 Jul;10(2):119-27. doi: 10.1006/nbdi.2002.0507.
3
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。
Environ Health Perspect. 2011 Jun;119(6):A259. doi: 10.1289/ehp.119-a259a.
4
Iron and paraquat as synergistic environmental risk factors in sporadic Parkinson's disease accelerate age-related neurodegeneration.铁和百草枯作为散发性帕金森病中协同作用的环境风险因素,会加速与年龄相关的神经退行性变。
J Neurosci. 2007 Jun 27;27(26):6914-22. doi: 10.1523/JNEUROSCI.1569-07.2007.
5
Multifactorial theory applied to the neurotoxicity of paraquat and paraquat-induced mechanisms of developing Parkinson's disease.多因素理论应用于百草枯的神经毒性及百草枯诱发帕金森病的发病机制。
Lab Invest. 2016 May;96(5):496-507. doi: 10.1038/labinvest.2015.161. Epub 2016 Feb 1.
6
Does paraquat cause Parkinson's disease? A review of reviews.百草枯是否会导致帕金森病?一篇综述的综述。
Neurotoxicology. 2021 Sep;86:180-184. doi: 10.1016/j.neuro.2021.08.006. Epub 2021 Aug 13.
7
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
Environ Toxicol. 2015 May-Jun;30(6):656-63. doi: 10.1002/tox.21943. Epub 2013 Dec 23.
8
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?
Eur J Neurosci. 2005 Sep;22(6):1294-304. doi: 10.1111/j.1460-9568.2005.04301.x.
9
Paraquat and Parkinson's disease.百草枯与帕金森病
Neurology. 1987 Nov;37(11):1820-1. doi: 10.1212/wnl.37.11.1820.
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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。
Science. 2013 Aug 16;341(6147):722-3. doi: 10.1126/science.1243619.

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Behavioral analysis of motor and non-motor impairment in rodent models of Parkinson's disease.帕金森病啮齿动物模型中运动和非运动障碍的行为分析。
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Cogs in the autophagic machine-equipped to combat dementia-prone neurodegenerative diseases.配备有对抗易患痴呆症的神经退行性疾病的自噬机制的组件。
Front Mol Neurosci. 2023 Aug 31;16:1225227. doi: 10.3389/fnmol.2023.1225227. eCollection 2023.
3
Clathrin-Dependent Uptake of Paraquat into SH-SY5Y Cells and Its Internalization into Different Subcellular Compartments.

本文引用的文献

1
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.
2
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.
3
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
百草枯通过网格蛋白依赖途径进入SH-SY5Y细胞及其在不同亚细胞区室的内化
Neurotox Res. 2017 Aug;32(2):204-217. doi: 10.1007/s12640-017-9722-0. Epub 2017 Mar 16.
4
Younger age at onset of sporadic Parkinson's disease among subjects occupationally exposed to metals and pesticides.职业接触金属和农药的人群中散发性帕金森病发病年龄较轻。
Interdiscip Toxicol. 2014 Sep;7(3):123-33. doi: 10.2478/intox-2014-0017. Epub 2014 Dec 30.
5
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。
Neurobiol Dis. 2014 Feb;62:172-8. doi: 10.1016/j.nbd.2013.09.019. Epub 2013 Oct 8.
6
Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson's, Huntington's, Alzheimer's, prions, bactericides, chemical toxicology and others as examples.从系统生物学角度理解配体结合不良的铁导致的大规模细胞死亡和破坏:以帕金森病、亨廷顿病、阿尔茨海默病、朊病毒、杀菌剂、化学毒理学等为例。
Arch Toxicol. 2010 Nov;84(11):825-89. doi: 10.1007/s00204-010-0577-x. Epub 2010 Aug 17.
7
Environmental exposure, obesity, and Parkinson's disease: lessons from fat and old worms.环境暴露、肥胖与帕金森病:从胖老线虫中得到的启示。
Environ Health Perspect. 2011 Jan;119(1):20-8. doi: 10.1289/ehp.1002522. Epub 2010 Aug 25.
8
Molecular mechanisms of pesticide-induced neurotoxicity: Relevance to Parkinson's disease.农药诱导神经毒性的分子机制:与帕金森病的关系。
Chem Biol Interact. 2010 Nov 5;188(2):289-300. doi: 10.1016/j.cbi.2010.06.003. Epub 2010 Jun 11.
9
Coupling endoplasmic reticulum stress to the cell death program in dopaminergic cells: effect of paraquat.将内质网应激与多巴胺能细胞中的细胞死亡程序相耦合:百草枯的作用
Neuromolecular Med. 2008;10(4):333-42. doi: 10.1007/s12017-008-8047-9. Epub 2008 Sep 5.
10
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。
Endocrine. 2006 Apr;29(2):275-87. doi: 10.1385/ENDO:29:2:275.
Neurobiol Dis. 2002 Jul;10(2):119-27. doi: 10.1006/nbdi.2002.0507.
4
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.
5
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.
6
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.
7
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.
8
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.
9
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.
10
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.