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Titolo:
Kainic acid induces selective mitochondrial oxidative phosphorylation enzyme dysfunction in cerebellar granule neurons: protective effects of melatonin and GSH ethyl ester
Autore:
Dabbeni-Sala, F; Floreani, M; Franceschini, D; Skaper, SD; Giusti, P;
Indirizzi:
Univ Padua, Dept Pharmacol, I-35131 Padua, Italy Univ Padua Padua Italy I-35131 dua, Dept Pharmacol, I-35131 Padua, Italy SmithKline Beecham Pharmaceut, Dept Neurosci Res, Harlow CM19 5AW, Essex, England SmithKline Beecham Pharmaceut Harlow Essex England CM19 5AW ssex, England
Titolo Testata:
FASEB JOURNAL
fascicolo: 8, volume: 15, anno: 2001,
pagine: NIL_378 - NIL_397
SICI:
0892-6638(200106)15:8<NIL_378:KAISMO>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
KAINATE-INDUCED EXCITOTOXICITY; BLUE-NATIVE-ELECTROPHORESIS; ELECTRON-TRANSPORT CHAIN; METHYL-D-ASPARTATE; PARKINSONS-DISEASE; RESPIRATORY-CHAIN; PRIMARY CULTURES; NITRIC-OXIDE; IN-VITRO; GLUTATHIONE DEPLETION;
Keywords:
neurotoxicity; mitochondrial respiratory chain; complex II; BN-PAGE analysis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Giusti, P Univ Padua, Dept Pharmacol, Largo E Meneghetti 2, I-35131 Padua,Italy Univ Padua Largo E Meneghetti 2 Padua Italy I-35131 adua, Italy
Citazione:
F. Dabbeni-Sala et al., "Kainic acid induces selective mitochondrial oxidative phosphorylation enzyme dysfunction in cerebellar granule neurons: protective effects of melatonin and GSH ethyl ester", FASEB J, 15(8), 2001, pp. NIL_378-NIL_397

Abstract

Kainic acid (KA), a potent central excitotoxin, may elicit neuronal death via generation of reactive oxygen species (ROS). The present study was undertaken to further characterize KA neurotoxicity and its relationship to ROSproduction and mitochondrial dysfunction. Exposure of rat cerebellar granule neurons at 14 days in vitro to 0.5 mM KA for 30 min resulted in the death of 53% of cells 24 h later. ROS production, evaluated by 2',7'-dichlorofluorescein diacetate, increased in KA-treated granule neurons. Resolution ofmitochondrial oxidative phosphorylation enzymes by blue native polyacrylamide gel electrophoresis, followed by histochemical staining, showed that KAinduced a strong decrease (-40%, P< 0.01) in succinate dehydrogenase (SDH)activity of complex II. Western analysis revealed a marked reduction in quantity of the catalytic portion of complex II enzyme in KA-treated cells. No significant changes were observed in the activities of other mitochondrial complex enzymes. The actions of KA at the mitochondrial level, as well ason ROS generation and cell viability, were prevented by the KA receptor-selective antagonist 6,7-dinitroquinoxaline-2,3(1H, 4H)-dione. Pretreatment of granule neurons with melatonin, a direct scavenger of ROS, or with the reduced glutathione (GSH) delivery agent GSH ethyl ester, before KA challengeprevented both the decrease in cell viability and complex II damage. The last result supports a link between KA-induced mitochondrial oxidative enzyme dysfunction and ROS generation. Together the results suggest mitochondriato be a critical target in KA injury to neurons.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 07:33:21