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Titolo:
Mitochondrial iron sequestration in dopamine-challenged astroglia: Role ofheme oxygenase-1 and the permeability transition pore
Autore:
Schipper, HM; Bernier, L; Mehindate, K; Frankel, D;
Indirizzi:
Siromfielder B Davis Jewish Hosp, Lady Davis Inst Med Res, Dept Neurol, Blo Sir Mortimer B Davis Jewish Hosp Montreal PQ Canada H3T 1E2 t Neurol, Blo McGill Univ, Dept Neurol & Neurosurg, Montreal, PQ, Canada McGill Univ Montreal PQ Canada Neurol & Neurosurg, Montreal, PQ, Canada McGill Univ, Dept Geriatr Med, Montreal, PQ, Canada McGill Univ Montreal PQ Canada v, Dept Geriatr Med, Montreal, PQ, Canada
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 5, volume: 72, anno: 1999,
pagine: 1802 - 1811
SICI:
0022-3042(199905)72:5<1802:MISIDA>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELLULAR STRESS MODEL; PARKINSONS-DISEASE; SUBSTANTIA-NIGRA; TRANSFERRIN RECEPTORS; LIPID-PEROXIDATION; OXIDATIVE STRESS; PRIMARY CULTURE; CYCLOSPORINE-A; NERVOUS-SYSTEM; BINDING-SITES;
Keywords:
astrocyte; heme oxygenase; iron; mitochondria; oxidative stress; Parkinson's disease; permeability transition pore;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Schipper, HM SiromfielderadaDavis Jewish Hosp, Lady Davis Inst Med Res, Dept Neurol, Blo Sir Mortimer B Davis Jewish Hosp 3755 Cote St Catherine Rd Montreal PQ Canada H3T 1E2
Citazione:
H.M. Schipper et al., "Mitochondrial iron sequestration in dopamine-challenged astroglia: Role ofheme oxygenase-1 and the permeability transition pore", J NEUROCHEM, 72(5), 1999, pp. 1802-1811

Abstract

Little is currently known concerning the mechanisms responsible for the excessive deposition of redox-active iron in the substantia nigra of subjectswith 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 trappingin 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-1inhibitors or modulators of the MTP) may afford effective neuroprotection in patients with PD and other neurological afflictions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 19:50:49