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Titolo:
MITOCHONDRIAL FREE-RADICAL SIGNAL IN CERAMIDE-DEPENDENT APOPTOSIS - APUTATIVE MECHANISM FOR NEURONAL DEATH IN PARKINSONS-DISEASE
Autore:
FRANCELANORD V; BRUGG B; MICHEL PP; AGID Y; RUBERG M;
Indirizzi:
HOP LA PITIE SALPETRIERE,INSERM U289,47 BLVD HOP F-75013 PARIS FRANCE HOP LA PITIE SALPETRIERE,INSERM U289 F-75013 PARIS FRANCE
Titolo Testata:
Journal of neurochemistry
fascicolo: 4, volume: 69, anno: 1997,
pagine: 1612 - 1621
SICI:
0022-3042(1997)69:4<1612:MFSICA>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; PROGRAMMED CELL-DEATH; NERVE GROWTH-FACTOR; NMDA RECEPTOR ACTIVATION; SUBSTANTIA-NIGRA; COMPLEX-I; GLUTATHIONE-PEROXIDASE; DOPAMINERGIC-NEURONS; SELECTIVE INCREASE; NITRIC-OXIDE;
Keywords:
PC12 CELLS; OXIDATIVE STRESS; SPHINGOMYELIN PATHWAY; SUPEROXIDE; NUCLEAR FACTOR KAPPA-B; FREE RADICALS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
69
Recensione:
Indirizzi per estratti:
Citazione:
V. Francelanord et al., "MITOCHONDRIAL FREE-RADICAL SIGNAL IN CERAMIDE-DEPENDENT APOPTOSIS - APUTATIVE MECHANISM FOR NEURONAL DEATH IN PARKINSONS-DISEASE", Journal of neurochemistry, 69(4), 1997, pp. 1612-1621

Abstract

Activation of the apoptogenic sphingomyelin-dependent signaling pathway in neuronally differentiated PC12 cells with cell-permeant C-2-ceramide resulted in a transient and short-lived emission of reactive oxygen species that was maximal 6 h after the beginning of treatment, followed immediately by nuclear translocation of the transcription factor nuclear factor kappa B. The production of reactive oxygen species was necessary for cell death to occur. The origin of the reactive oxygen species was identified as complex I of the mitochondrial electron transport chain. The mitochondria were not dysfunctional, however. They maintained normal membrane potentials and ATP synthesis until the cells began to die and the cell nuclei to condense and to fragment, similar to 12 h after the beginning of treatment. We conclude that a mitochondrial free radical signal plays a role in the sphingomyelin-dependent transduction pathway. Convergent data from postmortem brain suggest thatthis signaling pathway may be activated in the dopaminergic neurons that die in patients with Parkinson's disease and would provide a mechanism for oxidative stress implicating the mitochondria, both of which have long been hypothesized to play a role in the pathogenesis of thisdisease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/07/20 alle ore 22:19:13