ParkinsonFranceV1, PascalFrancis, Corpus, bibRecord, 001025

Influence of neuromelanin on oxidative pathways within the human substantia nigra

Identifieur interne : 001025 ( PascalFrancis/Corpus ); précédent : 001024; suivant : 001026

Influence of neuromelanin on oxidative pathways within the human substantia nigra

Auteurs : K. L. Double ; D. Ben-Shachar ; M. B. H. Youdim ; L. Zecca ; P. Riederer ; M. Gerlach

Source :

Neurotoxicology and teratology [ 0892-0362 ] ; 2002.

RBID : Pascal:03-0017999

Descripteurs français

Pascal (Inist)
- Mélanine, Neurone dopaminergique, Locus niger, Parkinson maladie, Homme, Etiologie, Pathogénie, Stress oxydatif.

English descriptors

KwdEn :
- Dopaminergic neuron, Etiology, Human, Locus niger, Melanin, Oxidative stress, Parkinson disease, Pathogenesis.

Abstract

Neuromelanin (NM) is a dark-coloured pigment produced in the dopaminergic neurons of the human substantia nigra (SN). The function of NM within the pigmented neurons is unknown but other melanins are believed to play a protective role via attenuation of free radical damage. Experimental evidence suggests that NM may also exhibit this characteristic, possibly by directly inactivating free radical species or via its ability to chelate transition metals, such as iron. Increased tissue iron, however, may saturate iron-chelating sites on NM and a looser association between iron and NM may result in an increased, rather than decreased, production of free radical species. The death of NM-pigmented neurons in Parkinson's disease (PD) is associated with both a measurable increase in tissue iron concentrations and indices of free radical mediated damage, suggesting that NM is involved in the aetiology of this disorder. As yet, it is unknown whether NM in the parkinsonian brain differs to that found in healthy tissue and thus may fulfil a different role within this tissue.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0892-0362`
A02	`01`			`@0 NETEEC`
A03		`1`		`@0 Neurotoxicol. teratol.`
A05				`@2 24`
A06				`@2 5`
A08	`01`	`1`	`ENG`	`@1 Influence of neuromelanin on oxidative pathways within the human substantia nigra`
A09	`01`	`1`	`ENG`	`@1 Milestones in Research on Neurotoxins and Neuroprotection: A Tribute to Professor Toshiharu Nagatsu`
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A11	`04`	`1`		`@1 ZECCA (L.)`
A11	`05`	`1`		`@1 RIEDERER (P.)`
A11	`06`	`1`		`@1 GERLACH (M.)`
A12	`01`	`1`		`@1 NAOI (Makoto) @9 ed.`
A12	`02`	`1`		`@1 PARVEZ (Hasan) @9 ed.`
A12	`03`	`1`		`@1 MARUYAMA (Wakako) @9 ed.`
A12	`04`	`1`		`@1 COLLINS (Michel A.) @9 ed.`
A12	`05`	`1`		`@1 YOUDIM (Moussa B. H.) @9 ed.`
A14	`01`			`@1 Prince of Wales Medical Research Institute, Barker Street @2 Randwick, Sydney, NSW 2031 @3 AUS @Z 1 aut.`
A14	`02`			`@1 Laboratory of Psychobiology, Department of Psychiatry Rambam Medical Centre, B. Rappaport Faculty of Medicine, Technion @2 Haifa @3 ISR @Z 2 aut.`
A14	`03`			`@1 Department of Pharmacology, B. Rappaport Faculty of Medicine, Eve Topf Neurodegenerative and National Parkinson Foundation Centres, Technion @2 Haifa @3 ISR @Z 3 aut.`
A14	`04`			`@1 Institute of Advanced Biomedical Technologies-CNR @2 Segrate @3 ITA @Z 4 aut.`
A14	`05`			`@1 Clinical Neurochemistry, Department of Psychiatry and Psychotherapy, University of Würzburg @2 97080 Würzburg @3 DEU @Z 5 aut.`
A14	`06`			`@1 Clinical Neurochemistry, Department of Child and Youth Psychiatry and Psychotherapy, University of Würzburg @2 Würzburg @3 DEU @Z 6 aut.`
A15	`01`			`@1 Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park @2 Mitake, Gifu 505-0116 @3 JPN @Z 1 aut.`
A15	`02`			`@1 Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS @2 91190 Gif sur Yvette @3 FRA @Z 2 aut.`
A15	`03`			`@1 Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences @2 Obu, Aichi 474-8622 @3 JPN @Z 3 aut.`
A15	`04`			`@1 Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine @2 Maywood, IL 60153 @3 USA @Z 4 aut.`
A15	`05`			`@1 Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion @2 Haifa 31096 @3 ISR @Z 5 aut.`
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C01	`01`		`ENG`	@0 Neuromelanin (NM) is a dark-coloured pigment produced in the dopaminergic neurons of the human substantia nigra (SN). The function of NM within the pigmented neurons is unknown but other melanins are believed to play a protective role via attenuation of free radical damage. Experimental evidence suggests that NM may also exhibit this characteristic, possibly by directly inactivating free radical species or via its ability to chelate transition metals, such as iron. Increased tissue iron, however, may saturate iron-chelating sites on NM and a looser association between iron and NM may result in an increased, rather than decreased, production of free radical species. The death of NM-pigmented neurons in Parkinson's disease (PD) is associated with both a measurable increase in tissue iron concentrations and indices of free radical mediated damage, suggesting that NM is involved in the aetiology of this disorder. As yet, it is unknown whether NM in the parkinsonian brain differs to that found in healthy tissue and thus may fulfil a different role within this tissue.
C02	`01`	`X`		`@0 002B17G`
C03	`01`	`X`	`FRE`	`@0 Mélanine @5 01`
C03	`01`	`X`	`ENG`	`@0 Melanin @5 01`
C03	`01`	`X`	`SPA`	`@0 Melanina @5 01`
C03	`02`	`X`	`FRE`	`@0 Neurone dopaminergique @5 04`
C03	`02`	`X`	`ENG`	`@0 Dopaminergic neuron @5 04`
C03	`02`	`X`	`SPA`	`@0 Neurona dopaminérgica @5 04`
C03	`03`	`X`	`FRE`	`@0 Locus niger @5 07`
C03	`03`	`X`	`ENG`	`@0 Locus niger @5 07`
C03	`03`	`X`	`SPA`	`@0 Locus níger @5 07`
C03	`04`	`X`	`FRE`	`@0 Parkinson maladie @5 10`
C03	`04`	`X`	`ENG`	`@0 Parkinson disease @5 10`
C03	`04`	`X`	`SPA`	`@0 Parkinson enfermedad @5 10`
C03	`05`	`X`	`FRE`	`@0 Homme @5 11`
C03	`05`	`X`	`ENG`	`@0 Human @5 11`
C03	`05`	`X`	`SPA`	`@0 Hombre @5 11`
C03	`06`	`X`	`FRE`	`@0 Etiologie @5 12`
C03	`06`	`X`	`ENG`	`@0 Etiology @5 12`
C03	`06`	`X`	`SPA`	`@0 Etiología @5 12`
C03	`07`	`X`	`FRE`	`@0 Pathogénie @5 13`
C03	`07`	`X`	`ENG`	`@0 Pathogenesis @5 13`
C03	`07`	`X`	`SPA`	`@0 Patogenia @5 13`
C03	`08`	`X`	`FRE`	`@0 Stress oxydatif @5 14`
C03	`08`	`X`	`ENG`	`@0 Oxidative stress @5 14`
C03	`08`	`X`	`SPA`	`@0 Estrés oxidativo @5 14`
C07	`01`	`X`	`FRE`	`@0 Système nerveux pathologie @5 61`
C07	`01`	`X`	`ENG`	`@0 Nervous system diseases @5 61`
C07	`01`	`X`	`SPA`	`@0 Sistema nervioso patología @5 61`
C07	`02`	`X`	`FRE`	`@0 Système nerveux central pathologie @5 62`
C07	`02`	`X`	`ENG`	`@0 Central nervous system disease @5 62`
C07	`02`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 62`
C07	`03`	`X`	`FRE`	`@0 Encéphale pathologie @5 63`
C07	`03`	`X`	`ENG`	`@0 Cerebral disorder @5 63`
C07	`03`	`X`	`SPA`	`@0 Encéfalo patología @5 63`
C07	`04`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 64`
C07	`04`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 64`
C07	`04`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 64`
C07	`05`	`X`	`FRE`	`@0 Maladie dégénérative @5 65`
C07	`05`	`X`	`ENG`	`@0 Degenerative disease @5 65`
C07	`05`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 65`
N21				`@1 006`
N82				`@1 PSI`

A30	`01`	`1`	`ENG`	`@1 International Catecholamine Symposium @2 9 @3 Kyoto JPN @4 2001-03-31`
A30	`02`	`1`	`ENG`	`@1 International Joint Congresses on Progress in Alzheimer's and Parkinson's Disease @2 5 @3 Kyoto JPN @4 2001-03-31`

Format Inist (serveur)

NO :	PASCAL 03-0017999 INIST
ET :	Influence of neuromelanin on oxidative pathways within the human substantia nigra
AU :	DOUBLE (K. L.); BEN-SHACHAR (D.); YOUDIM (M. B. H.); ZECCA (L.); RIEDERER (P.); GERLACH (M.); NAOI (Makoto); PARVEZ (Hasan); MARUYAMA (Wakako); COLLINS (Michel A.); YOUDIM (Moussa B. H.)
AF :	Prince of Wales Medical Research Institute, Barker Street/Randwick, Sydney, NSW 2031/Australie (1 aut.); Laboratory of Psychobiology, Department of Psychiatry Rambam Medical Centre, B. Rappaport Faculty of Medicine, Technion/Haifa/Israël (2 aut.); Department of Pharmacology, B. Rappaport Faculty of Medicine, Eve Topf Neurodegenerative and National Parkinson Foundation Centres, Technion/Haifa/Israël (3 aut.); Institute of Advanced Biomedical Technologies-CNR/Segrate/Italie (4 aut.); Clinical Neurochemistry, Department of Psychiatry and Psychotherapy, University of Würzburg/97080 Würzburg/Allemagne (5 aut.); Clinical Neurochemistry, Department of Child and Youth Psychiatry and Psychotherapy, University of Würzburg/Würzburg/Allemagne (6 aut.); Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park/Mitake, Gifu 505-0116/Japon (1 aut.); Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS/91190 Gif sur Yvette/France (2 aut.); Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences/Obu, Aichi 474-8622/Japon (3 aut.); Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine/Maywood, IL 60153/Etats-Unis (4 aut.); Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion/Haifa 31096/Israël (5 aut.)
DT :	Publication en série; Congrès; Niveau analytique
SO :	Neurotoxicology and teratology; ISSN 0892-0362; Coden NETEEC; Etats-Unis; Da. 2002; Vol. 24; No. 5; Pp. 621-628; Bibl. 67 ref.
LA :	Anglais
EA :	Neuromelanin (NM) is a dark-coloured pigment produced in the dopaminergic neurons of the human substantia nigra (SN). The function of NM within the pigmented neurons is unknown but other melanins are believed to play a protective role via attenuation of free radical damage. Experimental evidence suggests that NM may also exhibit this characteristic, possibly by directly inactivating free radical species or via its ability to chelate transition metals, such as iron. Increased tissue iron, however, may saturate iron-chelating sites on NM and a looser association between iron and NM may result in an increased, rather than decreased, production of free radical species. The death of NM-pigmented neurons in Parkinson's disease (PD) is associated with both a measurable increase in tissue iron concentrations and indices of free radical mediated damage, suggesting that NM is involved in the aetiology of this disorder. As yet, it is unknown whether NM in the parkinsonian brain differs to that found in healthy tissue and thus may fulfil a different role within this tissue.
CC :	002B17G
FD :	Mélanine; Neurone dopaminergique; Locus niger; Parkinson maladie; Homme; Etiologie; Pathogénie; Stress oxydatif
FG :	Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative
ED :	Melanin; Dopaminergic neuron; Locus niger; Parkinson disease; Human; Etiology; Pathogenesis; Oxidative stress
EG :	Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease
SD :	Melanina; Neurona dopaminérgica; Locus níger; Parkinson enfermedad; Hombre; Etiología; Patogenia; Estrés oxidativo
LO :	INIST-18910.354000109244300070
ID :	03-0017999

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Pascal:03-0017999

Le document en format XML

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<front><div type="abstract" xml:lang="en">Neuromelanin (NM) is a dark-coloured pigment produced in the dopaminergic neurons of the human substantia nigra (SN). The function of NM within the pigmented neurons is unknown but other melanins are believed to play a protective role via attenuation of free radical damage. Experimental evidence suggests that NM may also exhibit this characteristic, possibly by directly inactivating free radical species or via its ability to chelate transition metals, such as iron. Increased tissue iron, however, may saturate iron-chelating sites on NM and a looser association between iron and NM may result in an increased, rather than decreased, production of free radical species. The death of NM-pigmented neurons in Parkinson's disease (PD) is associated with both a measurable increase in tissue iron concentrations and indices of free radical mediated damage, suggesting that NM is involved in the aetiology of this disorder. As yet, it is unknown whether NM in the parkinsonian brain differs to that found in healthy tissue and thus may fulfil a different role within this tissue.</div>
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<fA14 i1="02"><s1>Laboratory of Psychobiology, Department of Psychiatry Rambam Medical Centre, B. Rappaport Faculty of Medicine, Technion</s1>
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<fA14 i1="03"><s1>Department of Pharmacology, B. Rappaport Faculty of Medicine, Eve Topf Neurodegenerative and National Parkinson Foundation Centres, Technion</s1>
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<sZ>3 aut.</sZ>
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<fA14 i1="04"><s1>Institute of Advanced Biomedical Technologies-CNR</s1>
<s2>Segrate</s2>
<s3>ITA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Clinical Neurochemistry, Department of Psychiatry and Psychotherapy, University of Würzburg</s1>
<s2>97080 Würzburg</s2>
<s3>DEU</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Clinical Neurochemistry, Department of Child and Youth Psychiatry and Psychotherapy, University of Würzburg</s1>
<s2>Würzburg</s2>
<s3>DEU</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA15 i1="01"><s1>Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park</s1>
<s2>Mitake, Gifu 505-0116</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
</fA15>
<fA15 i1="02"><s1>Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS</s1>
<s2>91190 Gif sur Yvette</s2>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
</fA15>
<fA15 i1="03"><s1>Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences</s1>
<s2>Obu, Aichi 474-8622</s2>
<s3>JPN</s3>
<sZ>3 aut.</sZ>
</fA15>
<fA15 i1="04"><s1>Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine</s1>
<s2>Maywood, IL 60153</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</fA15>
<fA15 i1="05"><s1>Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion</s1>
<s2>Haifa 31096</s2>
<s3>ISR</s3>
<sZ>5 aut.</sZ>
</fA15>
<fA20><s1>621-628</s1>
</fA20>
<fA21><s1>2002</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
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<fC01 i1="01" l="ENG"><s0>Neuromelanin (NM) is a dark-coloured pigment produced in the dopaminergic neurons of the human substantia nigra (SN). The function of NM within the pigmented neurons is unknown but other melanins are believed to play a protective role via attenuation of free radical damage. Experimental evidence suggests that NM may also exhibit this characteristic, possibly by directly inactivating free radical species or via its ability to chelate transition metals, such as iron. Increased tissue iron, however, may saturate iron-chelating sites on NM and a looser association between iron and NM may result in an increased, rather than decreased, production of free radical species. The death of NM-pigmented neurons in Parkinson's disease (PD) is associated with both a measurable increase in tissue iron concentrations and indices of free radical mediated damage, suggesting that NM is involved in the aetiology of this disorder. As yet, it is unknown whether NM in the parkinsonian brain differs to that found in healthy tissue and thus may fulfil a different role within this tissue.</s0>
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<fC03 i1="07" i2="X" l="SPA"><s0>Patogenia</s0>
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<fC03 i1="08" i2="X" l="FRE"><s0>Stress oxydatif</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Oxidative stress</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Estrés oxidativo</s0>
<s5>14</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>61</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>61</s5>
</fC07>
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<s5>62</s5>
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<s5>64</s5>
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<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>64</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>64</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>65</s5>
</fC07>
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<s5>65</s5>
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<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>65</s5>
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<fN21><s1>006</s1>
</fN21>
<fN82><s1>PSI</s1>
</fN82>
</pA>
<pR><fA30 i1="01" i2="1" l="ENG"><s1>International Catecholamine Symposium</s1>
<s2>9</s2>
<s3>Kyoto JPN</s3>
<s4>2001-03-31</s4>
</fA30>
<fA30 i1="02" i2="1" l="ENG"><s1>International Joint Congresses on Progress in Alzheimer's and Parkinson's Disease</s1>
<s2>5</s2>
<s3>Kyoto JPN</s3>
<s4>2001-03-31</s4>
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<server><NO>PASCAL 03-0017999 INIST</NO>
<ET>Influence of neuromelanin on oxidative pathways within the human substantia nigra</ET>
<AU>DOUBLE (K. L.); BEN-SHACHAR (D.); YOUDIM (M. B. H.); ZECCA (L.); RIEDERER (P.); GERLACH (M.); NAOI (Makoto); PARVEZ (Hasan); MARUYAMA (Wakako); COLLINS (Michel A.); YOUDIM (Moussa B. H.)</AU>
<AF>Prince of Wales Medical Research Institute, Barker Street/Randwick, Sydney, NSW 2031/Australie (1 aut.); Laboratory of Psychobiology, Department of Psychiatry Rambam Medical Centre, B. Rappaport Faculty of Medicine, Technion/Haifa/Israël (2 aut.); Department of Pharmacology, B. Rappaport Faculty of Medicine, Eve Topf Neurodegenerative and National Parkinson Foundation Centres, Technion/Haifa/Israël (3 aut.); Institute of Advanced Biomedical Technologies-CNR/Segrate/Italie (4 aut.); Clinical Neurochemistry, Department of Psychiatry and Psychotherapy, University of Würzburg/97080 Würzburg/Allemagne (5 aut.); Clinical Neurochemistry, Department of Child and Youth Psychiatry and Psychotherapy, University of Würzburg/Würzburg/Allemagne (6 aut.); Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park/Mitake, Gifu 505-0116/Japon (1 aut.); Unit of Neuroendocrinology, Bat. 5, Parc Chateau, CNRS/91190 Gif sur Yvette/France (2 aut.); Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute of Longevity Sciences/Obu, Aichi 474-8622/Japon (3 aut.); Department of Molecular and Cellular Biochemistry, Loyola University of Chicago, Strich School of Medicine/Maywood, IL 60153/Etats-Unis (4 aut.); Eve Topf and National Parkinson Foundation Neurodegenerative Diseases Centers, Department of Pharmacology, Rappaport Faculty of Medicine, Technion/Haifa 31096/Israël (5 aut.)</AF>
<DT>Publication en série; Congrès; Niveau analytique</DT>
<SO>Neurotoxicology and teratology; ISSN 0892-0362; Coden NETEEC; Etats-Unis; Da. 2002; Vol. 24; No. 5; Pp. 621-628; Bibl. 67 ref.</SO>
<LA>Anglais</LA>
<EA>Neuromelanin (NM) is a dark-coloured pigment produced in the dopaminergic neurons of the human substantia nigra (SN). The function of NM within the pigmented neurons is unknown but other melanins are believed to play a protective role via attenuation of free radical damage. Experimental evidence suggests that NM may also exhibit this characteristic, possibly by directly inactivating free radical species or via its ability to chelate transition metals, such as iron. Increased tissue iron, however, may saturate iron-chelating sites on NM and a looser association between iron and NM may result in an increased, rather than decreased, production of free radical species. The death of NM-pigmented neurons in Parkinson's disease (PD) is associated with both a measurable increase in tissue iron concentrations and indices of free radical mediated damage, suggesting that NM is involved in the aetiology of this disorder. As yet, it is unknown whether NM in the parkinsonian brain differs to that found in healthy tissue and thus may fulfil a different role within this tissue.</EA>
<CC>002B17G</CC>
<FD>Mélanine; Neurone dopaminergique; Locus niger; Parkinson maladie; Homme; Etiologie; Pathogénie; Stress oxydatif</FD>
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<ED>Melanin; Dopaminergic neuron; Locus niger; Parkinson disease; Human; Etiology; Pathogenesis; Oxidative stress</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease</EG>
<SD>Melanina; Neurona dopaminérgica; Locus níger; Parkinson enfermedad; Hombre; Etiología; Patogenia; Estrés oxidativo</SD>
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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Influence of neuromelanin on oxidative pathways within the human substantia nigra

Influence of neuromelanin on oxidative pathways within the human substantia nigra

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