Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease.
Identifieur interne : 001082 ( PubMed/Corpus ); précédent : 001081; suivant : 001083Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease.
Auteurs : Baptiste A. Faucheux ; Marie-Elise Martin ; Carole Beaumont ; Jean-Jacques Hauw ; Yves Agid ; Etienne C. HirschSource :
- Journal of neurochemistry [ 0022-3042 ] ; 2003.
English descriptors
- KwdEn :
- MESH :
- chemical , analysis : Ferric Compounds, Iron.
- chemical , metabolism : Iron, Melanins.
- metabolism : Substantia Nigra.
- pathology : Parkinson Disease, Substantia Nigra.
- Aged, Aged, 80 and over, Female, Humans, Macromolecular Substances, Male, Oxidation-Reduction, Prussian Blue Reaction.
Abstract
Degeneration of dopaminergic neurones during Parkinson's disease is most extensive in the subpopulation of melanized-neurones located in the substantia nigra pars compacta. Neuromelanin is a dark pigment produced in the dopaminergic neurones of the human substantia nigra and has the ability to bind a variety of metal ions, especially iron. Post-mortem analyses of the human brain have established that oxidative stress and iron content are enhanced in association with neuronal death. As redox-active iron (free Fe2+ form) and other transition metals have the ability to generate highly reactive hydroxyl radicals by a catalytic process, we investigated the redox activity of neuromelanin (NM)-aggregates in a group of parkinsonian patients, who presented a statistically significant reduction (- 70%) in the number of melanized-neurones and an increased non-heme (Fe3+) iron content as compared with a group of matched-control subjects. The level of redox activity detected in neuromelanin-aggregates was significantly increased (+ 69%) in parkinsonian patients and was highest in patients with the most severe neuronal loss. This change was not observed in tissue in the immediate vicinity of melanized-neurones. A possible consequence of an overloading of neuromelanin with redox-active elements is an increased contribution to oxidative stress and intraneuronal damage in patients with Parkinson's disease.
PubMed: 12911622
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Faucheux</name><affiliation><nlm:affiliation>INSERM U.289, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, F-75013 Paris, France. baptiste.faucheux@chups.jussieu.fr</nlm:affiliation></affiliation></author><author><name sortKey="Martin, Marie Elise" sort="Martin, Marie Elise" uniqKey="Martin M" first="Marie-Elise" last="Martin">Marie-Elise Martin</name></author><author><name sortKey="Beaumont, Carole" sort="Beaumont, Carole" uniqKey="Beaumont C" first="Carole" last="Beaumont">Carole Beaumont</name></author><author><name sortKey="Hauw, Jean Jacques" sort="Hauw, Jean Jacques" uniqKey="Hauw J" first="Jean-Jacques" last="Hauw">Jean-Jacques Hauw</name></author><author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. 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Faucheux</name><affiliation><nlm:affiliation>INSERM U.289, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, F-75013 Paris, France. baptiste.faucheux@chups.jussieu.fr</nlm:affiliation></affiliation></author><author><name sortKey="Martin, Marie Elise" sort="Martin, Marie Elise" uniqKey="Martin M" first="Marie-Elise" last="Martin">Marie-Elise Martin</name></author><author><name sortKey="Beaumont, Carole" sort="Beaumont, Carole" uniqKey="Beaumont C" first="Carole" last="Beaumont">Carole Beaumont</name></author><author><name sortKey="Hauw, Jean Jacques" sort="Hauw, Jean Jacques" uniqKey="Hauw J" first="Jean-Jacques" last="Hauw">Jean-Jacques Hauw</name></author><author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name></author></analytic><series><title level="j">Journal of neurochemistry</title><idno type="ISSN">0022-3042</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Ferric Compounds (analysis)</term><term>Humans</term><term>Iron (analysis)</term><term>Iron (metabolism)</term><term>Macromolecular Substances</term><term>Male</term><term>Melanins (metabolism)</term><term>Oxidation-Reduction</term><term>Parkinson Disease (pathology)</term><term>Prussian Blue Reaction</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Ferric Compounds</term><term>Iron</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Iron</term><term>Melanins</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Macromolecular Substances</term><term>Male</term><term>Oxidation-Reduction</term><term>Prussian Blue Reaction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Degeneration of dopaminergic neurones during Parkinson's disease is most extensive in the subpopulation of melanized-neurones located in the substantia nigra pars compacta. Neuromelanin is a dark pigment produced in the dopaminergic neurones of the human substantia nigra and has the ability to bind a variety of metal ions, especially iron. Post-mortem analyses of the human brain have established that oxidative stress and iron content are enhanced in association with neuronal death. As redox-active iron (free Fe2+ form) and other transition metals have the ability to generate highly reactive hydroxyl radicals by a catalytic process, we investigated the redox activity of neuromelanin (NM)-aggregates in a group of parkinsonian patients, who presented a statistically significant reduction (- 70%) in the number of melanized-neurones and an increased non-heme (Fe3+) iron content as compared with a group of matched-control subjects. The level of redox activity detected in neuromelanin-aggregates was significantly increased (+ 69%) in parkinsonian patients and was highest in patients with the most severe neuronal loss. This change was not observed in tissue in the immediate vicinity of melanized-neurones. A possible consequence of an overloading of neuromelanin with redox-active elements is an increased contribution to oxidative stress and intraneuronal damage in patients with Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12911622</PMID><DateCreated><Year>2003</Year><Month>08</Month><Day>12</Day></DateCreated><DateCompleted><Year>2003</Year><Month>11</Month><Day>12</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3042</ISSN><JournalIssue CitedMedium="Print"><Volume>86</Volume><Issue>5</Issue><PubDate><Year>2003</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Journal of neurochemistry</Title><ISOAbbreviation>J. Neurochem.</ISOAbbreviation></Journal><ArticleTitle>Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1142-8</MedlinePgn></Pagination><Abstract><AbstractText>Degeneration of dopaminergic neurones during Parkinson's disease is most extensive in the subpopulation of melanized-neurones located in the substantia nigra pars compacta. Neuromelanin is a dark pigment produced in the dopaminergic neurones of the human substantia nigra and has the ability to bind a variety of metal ions, especially iron. Post-mortem analyses of the human brain have established that oxidative stress and iron content are enhanced in association with neuronal death. As redox-active iron (free Fe2+ form) and other transition metals have the ability to generate highly reactive hydroxyl radicals by a catalytic process, we investigated the redox activity of neuromelanin (NM)-aggregates in a group of parkinsonian patients, who presented a statistically significant reduction (- 70%) in the number of melanized-neurones and an increased non-heme (Fe3+) iron content as compared with a group of matched-control subjects. The level of redox activity detected in neuromelanin-aggregates was significantly increased (+ 69%) in parkinsonian patients and was highest in patients with the most severe neuronal loss. This change was not observed in tissue in the immediate vicinity of melanized-neurones. A possible consequence of an overloading of neuromelanin with redox-active elements is an increased contribution to oxidative stress and intraneuronal damage in patients with Parkinson's disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Faucheux</LastName><ForeName>Baptiste A</ForeName><Initials>BA</Initials><AffiliationInfo><Affiliation>INSERM U.289, Hôpital de la Salpêtrière, 47 Boulevard de l'Hôpital, F-75013 Paris, France. baptiste.faucheux@chups.jussieu.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martin</LastName><ForeName>Marie-Elise</ForeName><Initials>ME</Initials></Author><Author ValidYN="Y"><LastName>Beaumont</LastName><ForeName>Carole</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Hauw</LastName><ForeName>Jean-Jacques</ForeName><Initials>JJ</Initials></Author><Author ValidYN="Y"><LastName>Agid</LastName><ForeName>Yves</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>Etienne C</ForeName><Initials>EC</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neurochem</MedlineTA><NlmUniqueID>2985190R</NlmUniqueID><ISSNLinking>0022-3042</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005290">Ferric Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D046911">Macromolecular Substances</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008543">Melanins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C014121">neuromelanin</NameOfSubstance></Chemical><Chemical><RegistryNumber>E1UOL152H7</RegistryNumber><NameOfSubstance UI="D007501">Iron</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005290" MajorTopicYN="N">Ferric Compounds</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007501" MajorTopicYN="N">Iron</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D046911" MajorTopicYN="N">Macromolecular Substances</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008543" MajorTopicYN="N">Melanins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011540" MajorTopicYN="N">Prussian Blue Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2003</Year><Month>8</Month><Day>13</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>11</Month><Day>13</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2003</Year><Month>8</Month><Day>13</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12911622</ArticleId><ArticleId IdType="pii">1923</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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