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Titolo:
Enantio-specific induction of apoptosis by an endogenous neurotoxin, N-methyl(R)salsolinol, in dopaminergic SH-SY5Y cells: suppression of apoptosis by N-(2-heptyl)-N-methylpropargylamine
Autore:
Maruyama, W; Boulton, AA; Davis, BA; Dostert, P; Naoi, M;
Indirizzi:
Inst Appl Biochem, Dept Brain Sci, Gifu 5050116, Japan Inst Appl Biochem Gifu Japan 5050116 Dept Brain Sci, Gifu 5050116, Japan Natl Inst Longev Sci, Dept Basic Gerontol, Lab Biochem & Metab, Aichi, Japan Natl Inst Longev Sci Aichi Japan tol, Lab Biochem & Metab, Aichi, Japan Univ Saskatchewan, Dept Psychiat, Neuropsychiat Res Unit, Saskatoon, SK S7N 0W0, Canada Univ Saskatchewan Saskatoon SK Canada S7N 0W0 skatoon, SK S7N 0W0, Canada Biotrial, Rennes, France Biotrial Rennes FranceBiotrial, Rennes, France
Titolo Testata:
JOURNAL OF NEURAL TRANSMISSION
fascicolo: 1, volume: 108, anno: 2001,
pagine: 11 - 24
SICI:
0300-9564(2001)108:1<11:EIOABA>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
OXIDASE-B INHIBITORS; ALIPHATIC N-METHYLPROPARGYLAMINES; PARKINSONS-DISEASE; METHYLTRANSFERASE ACTIVITY; NEURONS; PROPARGYLAMINES; 1(R),2(N)-DIMETHYL-6,7-DIHYDROXY-1,2,3,4-TETRAHYDROISOQUINOLINE; N-METHYL-(R)-SALSOLINOL; (R)SALSOLINOL; (-)-DEPRENYL;
Keywords:
Parkinson's disease; N-methyl(R)salsolinol; apoptosis; propargylamines; neuroprotection; mitochondrial membrane potential;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Naoi, M Inst Appl Biochem, Dept Brain Sci, Yagi Mem Pk, Gifu 5050116, Japan Inst Appl Biochem Yagi Mem Pk Gifu Japan 5050116 u 5050116, Japan
Citazione:
W. Maruyama et al., "Enantio-specific induction of apoptosis by an endogenous neurotoxin, N-methyl(R)salsolinol, in dopaminergic SH-SY5Y cells: suppression of apoptosis by N-(2-heptyl)-N-methylpropargylamine", J NEURAL TR, 108(1), 2001, pp. 11-24

Abstract

Endogenous N-methyl(R)salsolinol, which caused parkinsonism in rats by injection in the striatum, was found to induce apoptosis in dopaminergic neuroblastoma SH-SY5Y cells. After 12-h incubation with 500 muM N-methyl(R)salsolinol, almost all the cells died with apoptosis and necrotic cell death wasnegligible. N-Methyl(R)sasolinol was much more potent to induce apoptosis than the (S)-enantiomer. The mechanism of apoptosis was studied in relationto changes in mitochondrial membrane potential, Delta Psim, using a fluorescent indicator, JC-1. Red fluorescence of J-aggregates representing hyperpolarized Delta Psim was found to decrease significantly within 60min after incubation with N-methyl(li)salsolinol, but not by the (S)-enantiomer at the same concentration. It suggests that mitochondria may recognize the stereo-chemical structure of N-melhyl(R) salsolinol. Aliphatic propargylamines, (R)-N-(2-heptyl) -N-methylpropargylamine and (R)-N-(2-heptyl)propargylamine, were found to prevent Delta Psim loss and subsequent apoptosis induced byN-methyl(R)salsolinol. These results suggest that mitochondria play a key role in the induction of apoptosis by the neurotoxin and the prevention by aliphatic propargylamines.

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Documento generato il 08/08/20 alle ore 07:42:07