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

Identifieur interne : 003815 ( Main/Exploration ); précédent : 003814; suivant : 003816

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.

Affiliations:

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

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri