ParkinsonFranceV1, PascalFrancis, Curation, bibRecord, 000576

Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease

Identifieur interne : 000576 ( PascalFrancis/Curation ); précédent : 000575; suivant : 000577

Neuromelanin 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.

RBID : Pascal:04-0116693

Descripteurs français

Pascal (Inist)
- Fer, Locus niger, Dégénérescence, Neurone dopaminergique, Stress oxydatif, Mort cellulaire, Radical libre, Oxygène, Parkinson maladie, Homme, Neuromélanine.
Wicri :
- topic : Fer, Oxygène, Homme.

English descriptors

KwdEn :
- Cell death, Degeneration, Dopaminergic neuron, Free radical, Human, Iron, Locus niger, Neuromelanin, Oxidative stress, Oxygen, Parkinson disease.

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.

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A02	`01`			`@0 JONRA9`
A03		`1`		`@0 J. neurochem.`
A05				`@2 86`
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A08	`01`	`1`	`ENG`	`@1 Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease`
A11	`01`	`1`		`@1 FAUCHEUX (Baptiste A.)`
A11	`02`	`1`		`@1 MARTIN (Marie-Elise)`
A11	`03`	`1`		`@1 BEAUMONT (Carole)`
A11	`04`	`1`		`@1 HAUW (Jean-Jacques)`
A11	`05`	`1`		`@1 AGID (Yves)`
A11	`06`	`1`		`@1 HIRSCH (Etienne C.)`
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C01	`01`		`ENG`	@0 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.
C02	`01`	`X`		`@0 002B17G`
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C03	`01`	`X`	`ENG`	`@0 Iron @2 NC @5 01`
C03	`01`	`X`	`SPA`	`@0 Hierro @2 NC @5 01`
C03	`02`	`X`	`FRE`	`@0 Locus niger @5 02`
C03	`02`	`X`	`ENG`	`@0 Locus niger @5 02`
C03	`02`	`X`	`SPA`	`@0 Locus níger @5 02`
C03	`03`	`X`	`FRE`	`@0 Dégénérescence @5 03`
C03	`03`	`X`	`ENG`	`@0 Degeneration @5 03`
C03	`03`	`X`	`SPA`	`@0 Degeneración @5 03`
C03	`04`	`X`	`FRE`	`@0 Neurone dopaminergique @5 04`
C03	`04`	`X`	`ENG`	`@0 Dopaminergic neuron @5 04`
C03	`04`	`X`	`SPA`	`@0 Neurona dopaminérgica @5 04`
C03	`05`	`X`	`FRE`	`@0 Stress oxydatif @5 05`
C03	`05`	`X`	`ENG`	`@0 Oxidative stress @5 05`
C03	`05`	`X`	`SPA`	`@0 Estrés oxidativo @5 05`
C03	`06`	`X`	`FRE`	`@0 Mort cellulaire @5 06`
C03	`06`	`X`	`ENG`	`@0 Cell death @5 06`
C03	`06`	`X`	`SPA`	`@0 Muerte celular @5 06`
C03	`07`	`X`	`FRE`	`@0 Radical libre @2 FX @5 08`
C03	`07`	`X`	`ENG`	`@0 Free radical @2 FX @5 08`
C03	`07`	`X`	`SPA`	`@0 Radical libre @2 FX @5 08`
C03	`08`	`X`	`FRE`	`@0 Oxygène @2 NC @2 FX @5 10`
C03	`08`	`X`	`ENG`	`@0 Oxygen @2 NC @2 FX @5 10`
C03	`08`	`X`	`SPA`	`@0 Oxígeno @2 NC @2 FX @5 10`
C03	`09`	`X`	`FRE`	`@0 Parkinson maladie @5 12`
C03	`09`	`X`	`ENG`	`@0 Parkinson disease @5 12`
C03	`09`	`X`	`SPA`	`@0 Parkinson enfermedad @5 12`
C03	`10`	`X`	`FRE`	`@0 Homme @5 54`
C03	`10`	`X`	`ENG`	`@0 Human @5 54`
C03	`10`	`X`	`SPA`	`@0 Hombre @5 54`
C03	`11`	`X`	`FRE`	`@0 Neuromélanine @4 CD @5 96`
C03	`11`	`X`	`ENG`	`@0 Neuromelanin @4 CD @5 96`
C07	`01`	`X`	`FRE`	`@0 Encéphale pathologie @5 20`
C07	`01`	`X`	`ENG`	`@0 Cerebral disorder @5 20`
C07	`01`	`X`	`SPA`	`@0 Encéfalo patología @5 20`
C07	`02`	`X`	`FRE`	`@0 Système nerveux central @5 21`
C07	`02`	`X`	`ENG`	`@0 Central nervous system @5 21`
C07	`02`	`X`	`SPA`	`@0 Sistema nervioso central @5 21`
C07	`03`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 22`
C07	`03`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 22`
C07	`03`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 22`
C07	`04`	`X`	`FRE`	`@0 Maladie dégénérative @5 23`
C07	`04`	`X`	`ENG`	`@0 Degenerative disease @5 23`
C07	`04`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 23`
C07	`05`	`X`	`FRE`	`@0 Système nerveux central pathologie @5 24`
C07	`05`	`X`	`ENG`	`@0 Central nervous system disease @5 24`
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C07	`06`	`X`	`FRE`	`@0 Système nerveux pathologie @5 25`
C07	`06`	`X`	`ENG`	`@0 Nervous system diseases @5 25`
C07	`06`	`X`	`SPA`	`@0 Sistema nervioso patología @5 25`
N21				`@1 075`

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Le document en format XML

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<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>
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<fC01 i1="01" l="ENG"><s0>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.</s0>
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<fC03 i1="01" i2="X" l="ENG"><s0>Iron</s0>
<s2>NC</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Hierro</s0>
<s2>NC</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Locus niger</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Locus niger</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Locus níger</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Dégénérescence</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Degeneration</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Degeneración</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Neurone dopaminergique</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Dopaminergic neuron</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Neurona dopaminérgica</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Stress oxydatif</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Oxidative stress</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Estrés oxidativo</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Mort cellulaire</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Cell death</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Muerte celular</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Radical libre</s0>
<s2>FX</s2>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Free radical</s0>
<s2>FX</s2>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Radical libre</s0>
<s2>FX</s2>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Oxygène</s0>
<s2>NC</s2>
<s2>FX</s2>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Oxygen</s0>
<s2>NC</s2>
<s2>FX</s2>
<s5>10</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Oxígeno</s0>
<s2>NC</s2>
<s2>FX</s2>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>12</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>12</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Homme</s0>
<s5>54</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Human</s0>
<s5>54</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Hombre</s0>
<s5>54</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Neuromélanine</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Neuromelanin</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>25</s5>
</fC07>
<fN21><s1>075</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

La maladie de Parkinson en France (serveur d'exploration)

Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease

Neuromelanin associated redox-active iron is increased in the substantia nigra of patients with Parkinson's disease

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