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Titolo:
Neuroprotective effects of MK-801 on L-2-chloropropionic acid-induced neurotoxicity
Autore:
Williams, RE; Lock, EA; Bachelard, HS;
Indirizzi:
Zeneca Cent Toxicol Lab, Macclesfield SK10 4TJ, Cheshire, England Zeneca Cent Toxicol Lab Macclesfield Cheshire England SK10 4TJ e, England Univ Nottingham, Sch Phys & Astron, Magnet Resonance Ctr, Nottingham NG7 2RD, England Univ Nottingham Nottingham England NG7 2RD , Nottingham NG7 2RD, England
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 4, volume: 76, anno: 2001,
pagine: 1057 - 1065
SICI:
0022-3042(200102)76:4<1057:NEOMOL>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
NMDA ANTAGONIST MK-801; GRANULE CELL NECROSIS; SUCCINATE-DEHYDROGENASE; 3-NITROPROPIONIC ACID; RECEPTOR BLOCKADE; AMINO-ACIDS; RAT-BRAIN; EXCITOTOXICITY; NEURONS; NEUROPATHOLOGY;
Keywords:
cerebellar granule cells; L-2-chloropropionic acid; magnetic resonance spectroscopy; MK-801; pyruvate dehydrogenase activation; selective neurotoxicity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Williams, RE Zeneca Cent Toxicol Lab, Alderley Pk, Macclesfield SK10 4TJ, Cheshire, England Zeneca Cent Toxicol Lab Alderley Pk Macclesfield CheshireEngland SK10 4TJ
Citazione:
R.E. Williams et al., "Neuroprotective effects of MK-801 on L-2-chloropropionic acid-induced neurotoxicity", J NEUROCHEM, 76(4), 2001, pp. 1057-1065

Abstract

L-2-Chloropropionic acid is selectively toxic to the cerebellum in rats; the granule cell necrosis observed within 48 h can be prevented by prior administration of MK-801. Short-term treatment (2 h) with L-2-chloropropionic acid has also been shown to activate the mitochondrial pyruvate dehydrogenase complex in fasted adult rats. This study aimed to investigate the effectof prior exposure to MK-801 on the biochemical and neurotoxicological effects of L-2-chloropropionic acid. Extracts were prepared from the forebrain and cerebellum of animals that had been treated with L-2-chloropropionic acid, with and without prior treatment with MK-801, and were analysed using magnetic resonance spectroscopy and amino acid analysis. Glucose metabolism was studied by monitoring the metabolism of [1-C-13]-glucose using GC/MS. L-2-Chloropropionic acid caused increased glucose metabolism in both brain regions 6 h after administration, confirming activation of the pyruvate dehydrogenase complex, which was not prevented by MK-801. After 48 h an increase in lactate and a decrease in N-acetylaspartate was observed only in the cerebellum, whereas phosphocreatine and ATP decreased in both tissues. MK-801 prevented the changes in lactate and N-acetylaspartate, but not those on the energy state. These studies suggest that L-2-chloropropionic acid-induced neurotoxicity is only partly mediated by the NMDA subtype of glutamate receptor.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 00:56:42