Iron metabolism and Parkinson's disease.
Identifieur interne : 001490 ( PubMed/Corpus ); précédent : 001489; suivant : 001491Iron metabolism and Parkinson's disease.
Auteurs : E C Hirsch ; B A FaucheuxSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1998.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Hydroxyl Radical, Iron, Lactoferrin, Reactive Oxygen Species, Transferrin.
- chemical , physiology : Dopamine.
- pathology : Neurons, Parkinson Disease, Substantia Nigra.
- physiology : Cell Death.
- chemical : Free Radicals, Humans.
Abstract
There are at least three major reasons for thinking that iron participates in the mechanism of nerve cell death in Parkinson's disease (PD): (1) Iron catalyzes the formation of highly toxic hydroxyl radicals through the Fenton reaction. (2) Evidence suggests that oxidative stress participates in the mechanism of nerve cell death in PD. (3) Increased iron concentrations have been observed in the substantia nigra of patients with PD. In this review, we report data suggesting that the vulnerable neurons in PD are particularly sensitive to oxidative stress that may be induced by iron and then discuss the mechanisms by which iron levels may be increased in dopaminergic neurons in PD.
PubMed: 9613717
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pubmed:9613717Le document en format XML
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(2) Evidence suggests that oxidative stress participates in the mechanism of nerve cell death in PD. (3) Increased iron concentrations have been observed in the substantia nigra of patients with PD. In this review, we report data suggesting that the vulnerable neurons in PD are particularly sensitive to oxidative stress that may be induced by iron and then discuss the mechanisms by which iron levels may be increased in dopaminergic neurons in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9613717</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>Iron metabolism and Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>39-45</MedlinePgn></Pagination><Abstract><AbstractText>There are at least three major reasons for thinking that iron participates in the mechanism of nerve cell death in Parkinson's disease (PD): (1) Iron catalyzes the formation of highly toxic hydroxyl radicals through the Fenton reaction. (2) Evidence suggests that oxidative stress participates in the mechanism of nerve cell death in PD. (3) Increased iron concentrations have been observed in the substantia nigra of patients with PD. In this review, we report data suggesting that the vulnerable neurons in PD are particularly sensitive to oxidative stress that may be induced by iron and then discuss the mechanisms by which iron levels may be increased in dopaminergic neurons in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E C</ForeName><Initials>EC</Initials><AffiliationInfo><Affiliation>INSERM U289, Hôpital de la Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Faucheux</LastName><ForeName>B A</ForeName><Initials>BA</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</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="D005609">Free Radicals</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014168">Transferrin</NameOfSubstance></Chemical><Chemical><RegistryNumber>3352-57-6</RegistryNumber><NameOfSubstance UI="D017665">Hydroxyl Radical</NameOfSubstance></Chemical><Chemical><RegistryNumber>E1UOL152H7</RegistryNumber><NameOfSubstance UI="D007501">Iron</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.21.-</RegistryNumber><NameOfSubstance UI="D007781">Lactoferrin</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005609" MajorTopicYN="N">Free Radicals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017665" MajorTopicYN="N">Hydroxyl Radical</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007501" MajorTopicYN="N">Iron</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007781" MajorTopicYN="N">Lactoferrin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014168" MajorTopicYN="N">Transferrin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>55</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">9613717</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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