Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease
Identifieur interne : 003243 ( Main/Exploration ); précédent : 003242; suivant : 003244Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease
Auteurs : Baptiste A. Faucheux [France] ; Marie-Elise Martin [France] ; Carole Beaumont [France] ; Jean-Jacques Hauw [France] ; Yves Agid [France] ; Etienne C. Hirsch [France]Source :
- Journal of neurochemistry [ 0022-3042 ] ; 2003.
Descripteurs français
- Pascal (Inist)
- Wicri :
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Cell death, Degeneration, Dopaminergic neuron, Female, Ferric Compounds (analysis), Free radical, Human, Humans, Iron, Iron (analysis), Iron (metabolism), Locus niger, Macromolecular Substances, Male, Melanins (metabolism), Neuromelanin, Oxidation-Reduction, Oxidative stress, Oxygen, Parkinson Disease (pathology), Parkinson disease, Prussian Blue Reaction, Substantia Nigra (metabolism), Substantia Nigra (pathology).
- 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.
Affiliations:
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Faucheux</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>INSERM, U.289</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>U.360, Hôpital de la Saipêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Martin, Marie Elise" sort="Martin, Marie Elise" uniqKey="Martin M" first="Marie-Elise" last="Martin">Marie-Elise Martin</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>U.409, Faculté de Médecine X Bichat</s1><s2>Paris</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Beaumont, Carole" sort="Beaumont, Carole" uniqKey="Beaumont C" first="Carole" last="Beaumont">Carole Beaumont</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>U.409, Faculté de Médecine X Bichat</s1><s2>Paris</s2><s3>FRA</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Hauw, Jean Jacques" sort="Hauw, Jean Jacques" uniqKey="Hauw J" first="Jean-Jacques" last="Hauw">Jean-Jacques Hauw</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>U.360, Hôpital de la Saipêtrière</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>INSERM, U.289</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName><placeName><settlement type="city">Paris</settlement><region type="region" nuts="2">Île-de-France</region></placeName><orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName></affiliation></author><author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C." last="Hirsch">Etienne C. Hirsch</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>INSERM, U.289</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Île-de-France</region><region type="old region">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author></analytic><series><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno><imprint><date when="2003">2003</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Cell death</term><term>Degeneration</term><term>Dopaminergic neuron</term><term>Female</term><term>Ferric Compounds (analysis)</term><term>Free radical</term><term>Human</term><term>Humans</term><term>Iron</term><term>Iron (analysis)</term><term>Iron (metabolism)</term><term>Locus niger</term><term>Macromolecular Substances</term><term>Male</term><term>Melanins (metabolism)</term><term>Neuromelanin</term><term>Oxidation-Reduction</term><term>Oxidative stress</term><term>Oxygen</term><term>Parkinson Disease (pathology)</term><term>Parkinson disease</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><keywords scheme="Pascal" xml:lang="fr"><term>Fer</term><term>Locus niger</term><term>Dégénérescence</term><term>Neurone dopaminergique</term><term>Stress oxydatif</term><term>Mort cellulaire</term><term>Radical libre</term><term>Oxygène</term><term>Parkinson maladie</term><term>Homme</term><term>Neuromélanine</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Fer</term><term>Oxygène</term><term>Homme</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 Fe<sup>2+</sup> 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 (Fe<sup>3+</sup>) 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><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li></settlement><orgName><li>Hôpital de la Salpêtrière</li></orgName></list><tree><country name="France"><region name="Île-de-France"><name sortKey="Faucheux, Baptiste A" sort="Faucheux, Baptiste A" uniqKey="Faucheux B" first="Baptiste A." last="Faucheux">Baptiste A. Faucheux</name></region><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><name sortKey="Beaumont, Carole" sort="Beaumont, Carole" uniqKey="Beaumont C" first="Carole" last="Beaumont">Carole Beaumont</name><name sortKey="Faucheux, Baptiste A" sort="Faucheux, Baptiste A" uniqKey="Faucheux B" first="Baptiste A." last="Faucheux">Baptiste A. Faucheux</name><name sortKey="Hauw, Jean Jacques" sort="Hauw, Jean Jacques" uniqKey="Hauw J" first="Jean-Jacques" last="Hauw">Jean-Jacques Hauw</name><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C." last="Hirsch">Etienne C. Hirsch</name><name sortKey="Martin, Marie Elise" sort="Martin, Marie Elise" uniqKey="Martin M" first="Marie-Elise" last="Martin">Marie-Elise Martin</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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