Mechanisms of MPTP toxicity.
Identifieur interne : 004445 ( PubMed/Corpus ); précédent : 004444; suivant : 004446Mechanisms of MPTP toxicity.
Auteurs : S. Przedborski ; V. Jackson-LewisSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1998.
English descriptors
- KwdEn :
- Animals, Cell Death (drug effects), Disease Models, Animal, Dopamine (metabolism), Dopamine Agents (toxicity), Free Radicals, Humans, MPTP Poisoning, Mitochondria (drug effects), Nerve Degeneration (chemically induced), Parkinson Disease, Secondary (chemically induced), Substantia Nigra (drug effects).
- MESH :
- chemical , metabolism : Dopamine.
- chemically induced : Nerve Degeneration, Parkinson Disease, Secondary.
- drug effects : Cell Death, Mitochondria, Substantia Nigra.
- chemical , toxicity : Dopamine Agents.
- Animals, Disease Models, Animal, Free Radicals, Humans, MPTP Poisoning.
Abstract
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces an experimental model of Parkinson's disease (PD). It replicates most of the clinical features of PD as well as the main biochemical and pathologic hallmarks of the disease. Although the MPTP model departs from PD in several aspects, it is thought that important insights into the neurodegenerative process of PD may be obtained by elucidating the molecular mechanism of MPTP. In this article, we summarize the different steps of the complex metabolic pathway of MPTP and show how they may be implicated in predisposing individuals to PD. We also outline findings pertinent to the mode of action of MPTP including overproduction of free radicals, implication of nitric oxide, nitration of tyrosine, impairment of mitochondrial respiration, and occurrence of apoptosis. All of these factors may participate in the cascade of deleterious events that ultimately lead to the death of dopaminergic neurons after MPTP administration. Because of the similarity between PD and the MPTP model, we are speculating that a similar scenario may underlie the neurodegenerative process in PD.
PubMed: 9613716
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pubmed:9613716Le document en format XML
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Przedborski</name><affiliation><nlm:affiliation>Columbia University, Neurology Department, New York, NY 10032, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Jackson Lewis, V" sort="Jackson Lewis, V" uniqKey="Jackson Lewis V" first="V" last="Jackson-Lewis">V. Jackson-Lewis</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Death (drug effects)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Dopamine Agents (toxicity)</term><term>Free Radicals</term><term>Humans</term><term>MPTP Poisoning</term><term>Mitochondria (drug effects)</term><term>Nerve Degeneration (chemically induced)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Substantia Nigra (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Nerve Degeneration</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Death</term><term>Mitochondria</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Dopamine Agents</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Free Radicals</term><term>Humans</term><term>MPTP Poisoning</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces an experimental model of Parkinson's disease (PD). It replicates most of the clinical features of PD as well as the main biochemical and pathologic hallmarks of the disease. Although the MPTP model departs from PD in several aspects, it is thought that important insights into the neurodegenerative process of PD may be obtained by elucidating the molecular mechanism of MPTP. In this article, we summarize the different steps of the complex metabolic pathway of MPTP and show how they may be implicated in predisposing individuals to PD. We also outline findings pertinent to the mode of action of MPTP including overproduction of free radicals, implication of nitric oxide, nitration of tyrosine, impairment of mitochondrial respiration, and occurrence of apoptosis. All of these factors may participate in the cascade of deleterious events that ultimately lead to the death of dopaminergic neurons after MPTP administration. Because of the similarity between PD and the MPTP model, we are speculating that a similar scenario may underlie the neurodegenerative process in PD.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">9613716</PMID><DateCreated><Year>1998</Year><Month>08</Month><Day>06</Day></DateCreated><DateCompleted><Year>1998</Year><Month>08</Month><Day>06</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>13 Suppl 1</Volume><PubDate><Year>1998</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Mechanisms of MPTP toxicity.</ArticleTitle><Pagination><MedlinePgn>35-8</MedlinePgn></Pagination><Abstract><AbstractText>1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) produces an experimental model of Parkinson's disease (PD). It replicates most of the clinical features of PD as well as the main biochemical and pathologic hallmarks of the disease. Although the MPTP model departs from PD in several aspects, it is thought that important insights into the neurodegenerative process of PD may be obtained by elucidating the molecular mechanism of MPTP. In this article, we summarize the different steps of the complex metabolic pathway of MPTP and show how they may be implicated in predisposing individuals to PD. We also outline findings pertinent to the mode of action of MPTP including overproduction of free radicals, implication of nitric oxide, nitration of tyrosine, impairment of mitochondrial respiration, and occurrence of apoptosis. All of these factors may participate in the cascade of deleterious events that ultimately lead to the death of dopaminergic neurons after MPTP administration. Because of the similarity between PD and the MPTP model, we are speculating that a similar scenario may underlie the neurodegenerative process in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Przedborski</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Columbia University, Neurology Department, New York, NY 10032, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jackson-Lewis</LastName><ForeName>V</ForeName><Initials>V</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NS01724</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015259">Dopamine Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005609">Free Radicals</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016923">Cell Death</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D004195">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004298">Dopamine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015259">Dopamine Agents</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000633">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005609">Free Radicals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D020267">MPTP Poisoning</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008928">Mitochondria</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009410">Nerve Degeneration</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000139">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010302">Parkinson Disease, Secondary</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000139">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013378">Substantia Nigra</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>19</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>6</Month><Day>5</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>6</Month><Day>5</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1998</Year><Month>6</Month><Day>5</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9613716</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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