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Titolo:
EFFECTS OF VARIOUS TETRAHYDROISOQUINOLINE DERIVATIVES ON MITOCHONDRIAL RESPIRATION AND THE ELECTRON-TRANSFER COMPLEXES
Autore:
MORIKAWA N; NAOI M; MARUYAMA W; OHTA S; KOTAKE Y; KAWAI H; NIWA T; DOSTERT P; MIZUNO Y;
Indirizzi:
JUNTENDO UNIV,SCH MED,DEPT NEUROL,2-1-1 HONGO TOKYO 113 JAPAN JUNTENDO UNIV,SCH MED,DEPT NEUROL TOKYO 113 JAPAN NAGOYA INST TECHNOL,DEPT BIOSCI NAGOYA AICHI 466 JAPAN NATL INST LONGEV SCI,DEPT BASIC GERONTOL,BIOCHEM & METAB LAB OBU JAPAN UNIV TOKYO,FAC PHARMACEUT SCI,DEPT BIOORGAN & MED CHEM TOKYO JAPAN NAGOYA UNIV,BRANCH HOSP,DEPT INTERNAL MED NAGOYA AICHI JAPAN PHARMACIA & UPJOHN INC MILAN ITALY
Titolo Testata:
Journal of neural transmission
fascicolo: 6-7, volume: 105, anno: 1998,
pagine: 677 - 688
SICI:
0300-9564(1998)105:6-7<677:EOVTDO>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
BETA-CARBOLINIUM IONS; PARKINSONS-DISEASE; MOUSE-BRAIN; DOPAMINERGIC NEUROTOXIN; TYROSINE-HYDROXYLASE; MONOAMINE-OXIDASE; MASS-SPECTROMETRY; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; INHIBITION; RAT;
Keywords:
PARKINSONS DISEASE; MITOCHONDRIA; COMPLEX I; NEUROTOXINS; TETRAHYDROISOQUINOLINES; PATHOGENESIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
46
Recensione:
Indirizzi per estratti:
Citazione:
N. Morikawa et al., "EFFECTS OF VARIOUS TETRAHYDROISOQUINOLINE DERIVATIVES ON MITOCHONDRIAL RESPIRATION AND THE ELECTRON-TRANSFER COMPLEXES", Journal of neural transmission, 105(6-7), 1998, pp. 677-688

Abstract

We report effect of various tetrahydroisoquinoline derivatives on mitochondrial respiration and the electron transfer complexes. Generally these compounds were potent inhibitors of NADH-linked mitochondrial state 3 respiration and complex I. Presence of a phenyl group at the C1 position or oxidation of N-methylated isoquinones into N-methylisoquinolinium ion augmented the potency to inhibit mitochondrial respirationand complex I. Many of these compounds have been identified in human brains. In view of the mitochondrial and oxidative stress hypothesis, our results suggest involvement of these neurotoxins as potential causes of mitochondrial failure in Parkinson's disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 09:15:19