ParkinsonCanadaV1, PascalFrancis, Curation, bibRecord, 001164

Mitochondrial iron sequestration in dopamine-challenged astroglia : Role of heme oxygenase-1 and the permeability transition pore

Identifieur interne : 001164 ( PascalFrancis/Curation ); précédent : 001163; suivant : 001165

Mitochondrial iron sequestration in dopamine-challenged astroglia : Role of heme oxygenase-1 and the permeability transition pore

Auteurs : H. M. Schipper [Canada] ; L. Bernier [Canada] ; K. Mehindate [Canada] ; D. Frankel [Canada]

Source :

Journal of neurochemistry [ 0022-3042 ] ; 1999.

RBID : Pascal:99-0315872

Descripteurs français

Pascal (Inist)
- Fer, Dopamine, Heme oxygenase (decyclizing), Astrocyte, Perméabilité, Mitochondrie, Parkinson maladie, Rat, Stress oxydatif, In vitro.
Wicri :
- topic : Fer.

English descriptors

KwdEn :
- Astrocyte, Dopamine, Heme oxygenase (decyclizing), In vitro, Iron, Mitochondria, Oxidative stress, Parkinson disease, Permeability, Rat.

Abstract

Little is currently known concerning the mechanisms responsible for the excessive deposition of redox-active iron in the substantia nigra of subjects with Parkinson's disease (PD). In the present study, we demonstrate that dopamine promotes the selective sequestration of non-transferrin-derived iron by the mitochondrial compartment of cultured rat astroglia and that the mechanism underlying this novel dopamine effect is oxidative in nature. We also provide evidence that up-regulation of the stress protein heme oxygenase-1 (HO-1) is both necessary and sufficient for mitochondrial iron trapping in dopamine-challenged astroglia. Finally, we show that opening of the mitochondrial transition pore (MTP) mediates the influx of non-transferrin-derived iron into mitochondria of dopamine-stimulated and HO-1-transfected astroglia. Our findings provide an explanation for the pathological iron sequestration, mitochondrial insufficiency, and amplification of oxidative injury reported in the brains of PD subjects. Pharmacological blockade of transition metal trapping by "stressed" astroglial mitochondria (e.g., using HO-1 inhibitors or modulators of the MTP) may afford effective neuroprotection in patients with PD and other neurological afflictions.

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A08	`01`	`1`	`ENG`	`@1 Mitochondrial iron sequestration in dopamine-challenged astroglia : Role of heme oxygenase-1 and the permeability transition pore`
A11	`01`	`1`		`@1 SCHIPPER (H. M.)`
A11	`02`	`1`		`@1 BERNIER (L.)`
A11	`03`	`1`		`@1 MEHINDATE (K.)`
A11	`04`	`1`		`@1 FRANKEL (D.)`
A14	`01`			`@1 Bloomfield Centre for Research in Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital @2 Montreal, Quebec @3 CAN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut.`
A14	`02`			`@1 Departments of Neurology and Neurosurgery and Medicine (Geriatrics), McGill University @2 Montreal, Quebec @3 CAN @Z 1 aut. @Z 4 aut.`
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A21				`@1 1999`
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C01	`01`		`ENG`	@0 Little is currently known concerning the mechanisms responsible for the excessive deposition of redox-active iron in the substantia nigra of subjects with Parkinson's disease (PD). In the present study, we demonstrate that dopamine promotes the selective sequestration of non-transferrin-derived iron by the mitochondrial compartment of cultured rat astroglia and that the mechanism underlying this novel dopamine effect is oxidative in nature. We also provide evidence that up-regulation of the stress protein heme oxygenase-1 (HO-1) is both necessary and sufficient for mitochondrial iron trapping in dopamine-challenged astroglia. Finally, we show that opening of the mitochondrial transition pore (MTP) mediates the influx of non-transferrin-derived iron into mitochondria of dopamine-stimulated and HO-1-transfected astroglia. Our findings provide an explanation for the pathological iron sequestration, mitochondrial insufficiency, and amplification of oxidative injury reported in the brains of PD subjects. Pharmacological blockade of transition metal trapping by "stressed" astroglial mitochondria (e.g., using HO-1 inhibitors or modulators of the MTP) may afford effective neuroprotection in patients with PD and other neurological afflictions.
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C03	`02`	`X`	`SPA`	`@0 Dopamina @2 NK @2 FR @5 02`
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C03	`03`	`X`	`ENG`	`@0 Heme oxygenase (decyclizing) @2 FE @5 03`
C03	`03`	`X`	`SPA`	`@0 Heme oxygenase (decyclizing) @2 FE @5 03`
C03	`04`	`X`	`FRE`	`@0 Astrocyte @5 04`
C03	`04`	`X`	`ENG`	`@0 Astrocyte @5 04`
C03	`04`	`X`	`SPA`	`@0 Astrocito @5 04`
C03	`05`	`X`	`FRE`	`@0 Perméabilité @5 07`
C03	`05`	`X`	`ENG`	`@0 Permeability @5 07`
C03	`05`	`X`	`SPA`	`@0 Permeabilidad @5 07`
C03	`06`	`X`	`FRE`	`@0 Mitochondrie @5 08`
C03	`06`	`X`	`ENG`	`@0 Mitochondria @5 08`
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C03	`08`	`X`	`SPA`	`@0 Rata @5 69`
C03	`09`	`X`	`FRE`	`@0 Stress oxydatif @5 70`
C03	`09`	`X`	`ENG`	`@0 Oxidative stress @5 70`
C03	`09`	`X`	`SPA`	`@0 Stress oxidativo @5 70`
C03	`10`	`X`	`FRE`	`@0 In vitro @5 72`
C03	`10`	`X`	`ENG`	`@0 In vitro @5 72`
C03	`10`	`X`	`SPA`	`@0 In vitro @5 72`
C07	`01`	`X`	`FRE`	`@0 Oxidoreductases @2 FE`
C07	`01`	`X`	`ENG`	`@0 Oxidoreductases @2 FE`
C07	`01`	`X`	`SPA`	`@0 Oxidoreductases @2 FE`
C07	`02`	`X`	`FRE`	`@0 Enzyme`
C07	`02`	`X`	`ENG`	`@0 Enzyme`
C07	`02`	`X`	`SPA`	`@0 Enzima`
C07	`03`	`X`	`FRE`	`@0 Neurotransmetteur @5 23`
C07	`03`	`X`	`ENG`	`@0 Neurotransmitter @5 23`
C07	`03`	`X`	`SPA`	`@0 Neurotransmisor @5 23`
C07	`04`	`X`	`FRE`	`@0 Catécholamine @5 24`
C07	`04`	`X`	`ENG`	`@0 Catecholamine @5 24`
C07	`04`	`X`	`SPA`	`@0 Catecolamina @5 24`
C07	`05`	`X`	`FRE`	`@0 Névroglie @5 29`
C07	`05`	`X`	`ENG`	`@0 Neuroglia @5 29`
C07	`05`	`X`	`SPA`	`@0 Neuroglia @5 29`
C07	`06`	`X`	`FRE`	`@0 Système nerveux pathologie @5 38`
C07	`06`	`X`	`ENG`	`@0 Nervous system diseases @5 38`
C07	`06`	`X`	`SPA`	`@0 Sistema nervioso patología @5 38`
C07	`07`	`X`	`FRE`	`@0 Système nerveux central pathologie @5 39`
C07	`07`	`X`	`ENG`	`@0 Central nervous system disease @5 39`
C07	`07`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 39`
C07	`08`	`X`	`FRE`	`@0 Encéphale pathologie @5 40`
C07	`08`	`X`	`ENG`	`@0 Cerebral disorder @5 40`
C07	`08`	`X`	`SPA`	`@0 Encéfalo patología @5 40`
C07	`09`	`X`	`FRE`	`@0 Extrapyramidal syndrome @5 41`
C07	`09`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 41`
C07	`09`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 41`
C07	`10`	`X`	`FRE`	`@0 Maladie dégénérative @5 42`
C07	`10`	`X`	`ENG`	`@0 Degenerative disease @5 42`
C07	`10`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 42`
C07	`11`	`X`	`FRE`	`@0 Rodentia @2 NS`
C07	`11`	`X`	`ENG`	`@0 Rodentia @2 NS`
C07	`11`	`X`	`SPA`	`@0 Rodentia @2 NS`
C07	`12`	`X`	`FRE`	`@0 Mammalia @2 NS`
C07	`12`	`X`	`ENG`	`@0 Mammalia @2 NS`
C07	`12`	`X`	`SPA`	`@0 Mammalia @2 NS`
C07	`13`	`X`	`FRE`	`@0 Vertebrata @2 NS`
C07	`13`	`X`	`ENG`	`@0 Vertebrata @2 NS`
C07	`13`	`X`	`SPA`	`@0 Vertebrata @2 NS`
N21				`@1 200`

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Pascal:99-0315872

Le document en format XML

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<front><div type="abstract" xml:lang="en">Little is currently known concerning the mechanisms responsible for the excessive deposition of redox-active iron in the substantia nigra of subjects with Parkinson's disease (PD). In the present study, we demonstrate that dopamine promotes the selective sequestration of non-transferrin-derived iron by the mitochondrial compartment of cultured rat astroglia and that the mechanism underlying this novel dopamine effect is oxidative in nature. We also provide evidence that up-regulation of the stress protein heme oxygenase-1 (HO-1) is both necessary and sufficient for mitochondrial iron trapping in dopamine-challenged astroglia. Finally, we show that opening of the mitochondrial transition pore (MTP) mediates the influx of non-transferrin-derived iron into mitochondria of dopamine-stimulated and HO-1-transfected astroglia. Our findings provide an explanation for the pathological iron sequestration, mitochondrial insufficiency, and amplification of oxidative injury reported in the brains of PD subjects. Pharmacological blockade of transition metal trapping by "stressed" astroglial mitochondria (e.g., using HO-1 inhibitors or modulators of the MTP) may afford effective neuroprotection in patients with PD and other neurological afflictions.</div>
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<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Heme oxygenase (decyclizing)</s0>
<s2>FE</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Heme oxygenase (decyclizing)</s0>
<s2>FE</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Heme oxygenase (decyclizing)</s0>
<s2>FE</s2>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Astrocyte</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Astrocyte</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Astrocito</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Perméabilité</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Permeability</s0>
<s5>07</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Permeabilidad</s0>
<s5>07</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Mitochondrie</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Mitochondria</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Mitocondria</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Rat</s0>
<s5>69</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Rat</s0>
<s5>69</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Rata</s0>
<s5>69</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Stress oxydatif</s0>
<s5>70</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Oxidative stress</s0>
<s5>70</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Stress oxidativo</s0>
<s5>70</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>In vitro</s0>
<s5>72</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>In vitro</s0>
<s5>72</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>In vitro</s0>
<s5>72</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>23</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>23</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>24</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>24</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Névroglie</s0>
<s5>29</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Neuroglia</s0>
<s5>29</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Neuroglia</s0>
<s5>29</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>42</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>42</s5>
</fC07>
<fC07 i1="11" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="11" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="11" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="12" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="12" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="12" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="13" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="13" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="13" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21><s1>200</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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   |texte=   Mitochondrial iron sequestration in dopamine-challenged astroglia : Role of heme oxygenase-1 and the permeability transition pore
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This area was generated with Dilib version V0.6.29.
Data generation: Thu May 4 22:20:19 2017. Site generation: Fri Dec 23 23:17:26 2022

	La maladie de Parkinson au Canada (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 au Canada (serveur d'exploration)

Mitochondrial iron sequestration in dopamine-challenged astroglia : Role of heme oxygenase-1 and the permeability transition pore

Mitochondrial iron sequestration in dopamine-challenged astroglia : Role of heme oxygenase-1 and the permeability transition pore

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