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Titolo:
Mitochondria deficient in complex I activity are depolarized by hydrogen peroxide in nerve terminals: relevance to Parkinson's disease
Autore:
Chinopoulos, C; Adam-Vizi, V;
Indirizzi:
Semmelweis Univ Med, Dept Med Biochem, H-1444 Budapest, Hungary SemmelweisUniv Med Budapest Hungary H-1444 em, H-1444 Budapest, Hungary
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 1, volume: 76, anno: 2001,
pagine: 302 - 306
SICI:
0022-3042(200101)76:1<302:MDICIA>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
ELECTRON-TRANSPORT CHAIN; OXIDATIVE STRESS; BRAIN MITOCHONDRIA; SYNAPTOSOMES; ENERGY; INHIBITION; RAT; 1-METHYL-4-PHENYLPYRIDINIUM; INVOLVEMENT; RESPIRATION;
Keywords:
complex I; hydrogen peroxide; mitochondria; mitochondrial membrane potential; oxidative stress; Parkinson's disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Adam-Vizi, V Semmelweis Univ Med, Dept Med Biochem, POB 262, H-1444 Budapest, Hungary Semmelweis Univ Med POB 262 Budapest Hungary H-1444 Hungary
Citazione:
C. Chinopoulos e V. Adam-Vizi, "Mitochondria deficient in complex I activity are depolarized by hydrogen peroxide in nerve terminals: relevance to Parkinson's disease", J NEUROCHEM, 76(1), 2001, pp. 302-306

Abstract

Deficiency of complex I in the respiratory chain and oxidative stress induced by hydrogen peroxide occur simultaneously in dopaminergic neurones in Parkinson's disease. Here we demonstrate that the membrane potential of in sif(I mitochondria (Delta Psim), as measured by the fluorescence change of JC-I (5,5',6,6'-tetrachloro-1,1,3,3'-tetraethylbenzimidazolylcarbocyanine iodide), collapses when isolated nerve terminals are exposed to hydrogen peroxide (H2O2,100 and 500 muM) in combination with the inhibition of complex Iby rotenone (5 nM-1 muM). H2O2 reduced the activity of complex I by 17%, and the effect of H2O2 and rotenone on the enzyme was found to be additive. A decrease in Delta Psim induced by H2O2 was significant when the activity of complex I was reduced to a similar extent as found in Parkinson's disease (26%). The loss of Delta Psim observed in the combined presence of complex I deficiency and H2O2 indicates that when complex I is partially inhibited, mitochondria in nerve terminals become more vulnerable to H2O2-induced oxidative stress. This mechanism could be crucial in the development of bioenergetic failure in Parkinson's disease.

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Documento generato il 22/01/20 alle ore 07:15:14