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Titolo:
2-DEOXYGLUCOSE ENHANCES METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE-INDUCED ATP LOSS IN THE MOUSE-BRAIN
Autore:
CHAN P; LANGSTON JW; IRWIN I; DELANNEY LE; DIMONTE DA;
Indirizzi:
CALIF INST MED RES,2260 CLOVE DR SAN JOSE CA 95128 CALIF PARKINSONS FDN SAN JOSE CA 00000
Titolo Testata:
Journal of neurochemistry
fascicolo: 2, volume: 61, anno: 1993,
pagine: 610 - 616
SICI:
0022-3042(1993)61:2<610:2EM>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
PRIMARY CULTURES; NEUROTOXIN 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; 1-METHYL-4-PHENYLPYRIDINIUM ION; ISOLATED HEPATOCYTES; CELLULAR-RESISTANCE; MPTP NEUROTOXICITY; DOPAMINE NEURONS; TOXICITY; MPP+; INHIBITION;
Keywords:
1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; 1-METHYL-4-PHENYLPYRIDINIUM; ATP; 2-DEOXYGLUCOSE; ENERGY METABOLISM; PARKINSONISM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
P. Chan et al., "2-DEOXYGLUCOSE ENHANCES METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE-INDUCED ATP LOSS IN THE MOUSE-BRAIN", Journal of neurochemistry, 61(2), 1993, pp. 610-616

Abstract

The effects of 2-deoxyglucose (2-DG), an inhibitor of the uptake and use of glucose, on ATP loss caused by the neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) were determined in the mouse brain. 2-DG alone had no effect on brain ATP levels, but when administered 30 min before MPTP exposure, 2-DG significantly enhanced MPTP-induced ATP reduction. This was reflected as an increase in ATP loss in the striatum (from 15 to 27%) as well as a significant decrease in ATP in the cerebellar cortex, an area of the brain that was not affected after exposure to MPTP alone. In mice pretreated with 2-DG, striatal ATP levels remained significantly decreased for >8 h after MPTP administration. In contrast, ATP levels in the cerebellar cortex returned to normal values within 4 h from MPTP exposure. Mazindol, a catecholamine uptake blocker, completely protected against MPTP-induced loss of striatal ATP in the absence of 2-DG, but it only partially prevented striatalATP decrease after administration of both 2-DG and MPTP; mazindol wasalso ineffective in protecting against ATP loss caused by 2-DG and MPTP in the cerebellar cortex. 2-DG/MPTP-induced ATP loss appeared to beassociated with the presence of the 1-methyl-4-phenylpyridinium (MPP+) metabolite because (1) the pattern of ATP recovery in the striatum and cerebellar cortex appeared to reflect the pattern of MPP+ clearancefrom these areas of the brain (i.e., significant MPP+ levels persisted longer in the striatum than in the cerebellar cortex), and (2) ATP decrease was completely prevented by blocking the conversion of MPTP toMPP+ with the monoamine oxidase B inhibitor deprenyl. Data indicate that impairment of glucose metabolism dramatically enhances the effectsof MPTP/MPP+ on cerebral energy supplies, making these effects relatively nonselective for dopaminergic neurons of the nigrostriatal pathway.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 15:39:31