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Titolo:
ENERGY THRESHOLDS IN BRAIN MITOCHONDRIA - POTENTIAL INVOLVEMENT IN NEURODEGENERATION
Autore:
DAVEY GP; PEUCHEN S; CLARK JB;
Indirizzi:
TRINITY COLL DUBLIN,DEPT BIOCHEM DUBLIN 2 IRELAND INST NEUROL,DEPT NEUROCHEM LONDON WC1N 3BG ENGLAND
Titolo Testata:
The Journal of biological chemistry
fascicolo: 21, volume: 273, anno: 1998,
pagine: 12753 - 12757
SICI:
0021-9258(1998)273:21<12753:ETIBM->2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
COMPLEX-I DEFICIENCY; OXIDATIVE-PHOSPHORYLATION; PARKINSONS-DISEASE; GLUTATHIONE DEFICIENCY; CYTOCHROME-OXIDASE; ALZHEIMERS-DISEASE; NEURONAL DEATH; RAT-BRAIN; RESPIRATION; CELL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
59
Recensione:
Indirizzi per estratti:
Citazione:
G.P. Davey et al., "ENERGY THRESHOLDS IN BRAIN MITOCHONDRIA - POTENTIAL INVOLVEMENT IN NEURODEGENERATION", The Journal of biological chemistry, 273(21), 1998, pp. 12753-12757

Abstract

Decreases in mitochondrial respiratory chain complex activities have been implicated in neurodegenerative disorders such as Parkinson's disease, Huntington's disease, and Alzheimer's disease, However, the extent to which these decreases cause a disturbance in oxidative phosphorylation and energy homeostasis in the brain is not known. We therefore examined the relative contribution of individual mitochondrial respiratory chain complexes to the control of NAD-linked substrate oxidative phosphorylation in synaptic mitochondria. Titration of complex I, III,and IV activities with specific inhibitors generated threshold curvesthat showed the extent to which a complex activity could be inhibitedbefore causing impairment of mitochondrial energy metabolism. ComplexI, III, and TV activities were decreased by approximately 25, 80, and70%, respectively, before major changes in rates of oxygen consumption and ATP synthesis mere observed. These results suggest that, in mitochondria of synaptic origin, complex I activity has a major control ofoxidative phosphorylation, such that when a threshold of 25% inhibition is exceeded, energy metabolism is severely impaired, resulting in areduced synthesis of ATP. Additionally, depletion of glutathione, which has been reported to be a primary event in idiopathic Parkinson's disease, eliminated the complex I threshold in PC12 cells, suggesting that antioxidant status is important in maintaining energy thresholds in mitochondria. The implications of these findings are discussed with respect to neurodegenerative disorders and energy metabolism in the synapse.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 10:19:50