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Titolo:
Involvement of endogenous N-methyl(R) salsolinol in Parkinson's disease: induction of apoptosis and protection by (-)deprenyl
Autore:
Naoi, M; Maruyama, W; Takahashi, T; Akao, Y; Nakagawa, Y;
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, Biochem & Metab Lab, Aichi, Japan Natl Inst Longev Sci Aichi Japan tol, Biochem & Metab Lab, Aichi, Japan Aichi Konan Coll, Dept Food & Nutr, Aichi, Japan Aichi Konan Coll Aichi Japan Konan Coll, Dept Food & Nutr, Aichi, Japan Gifu Int Inst Biotechnol, Gifu, Japan Gifu Int Inst Biotechnol Gifu Japan fu Int Inst Biotechnol, Gifu, Japan Osaka Med Coll, Dept Internal Med 2, Takatsuki, Osaka 569, Japan Osaka MedColl Takatsuki Osaka Japan 569 d 2, Takatsuki, Osaka 569, Japan
Titolo Testata:
JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT
fascicolo: 58, , anno: 2000,
pagine: 111 - 121
SICI:
0303-6995(2000):58<111:IOENSI>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
NEUROBLASTOMA SH-SY5Y CELLS; N-METHYLTRANSFERASE ACTIVITY; DOPAMINERGIC NEUROTOXIN; 1,2(N)-DIMETHYL-6,7-DIHYDROXYISOQUINOLINIUM ION; DEPRENYL; RAT; INCREASES; NEURONS; DEATH; 1(R),2(N)-DIMETHYL-6,7-DIHYDROXY-1,2,3,4-TETRAHYDROISOQUINOLINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
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:
M. Naoi et al., "Involvement of endogenous N-methyl(R) salsolinol in Parkinson's disease: induction of apoptosis and protection by (-)deprenyl", J NEUR TR-S, (58), 2000, pp. 111-121

Abstract

An endogenous dopamine-derived N-methyl(R)salsolinol has been suggested tobe involved in the pathogenesis of Parkinson's disease. In Parkinson's disease, the level of N-methyl(R)salsolinol increased in cerebrospinal fluid and the high activity of a synthesizing enzyme, (R)salsolinol N-methyltransferase, was detected in lymphocytes. This isoquinoline induced apoptotic DNAdamage in human dopaminergic neuroblastoma SH-SY5Y cells. Among catechol isoquinolines, only N-methylsalsolinol induced apoptosis in the cells, and the scavengers of hydroxyl radicals and antioxidants suppressed DNA damage, suggesting that reactive oxygen species initiate apoptosis. The isoquinoline activated caspase-3 like proteases and a caspase-3 inhibitor protected the cells from DNA damage. (-)Deprenyl, but neither clorgyline nor pargyline,prevented apoptotic cell death. The mechanism of the protection was due tostabilization of mitochondrial membrane potential reduced by the toxin. InParkinson's disease apoptosis may be induced in dopamine neurons by this endogenous neurotoxin, and (-)deprenyl may protect them from apoptotic deathprocess.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 02:05:41