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BDNF or IGF-I potentiates free radical-mediated injury in cortical cell cultures.

Authors
Gwag, BJ; Koh, JY; Chen, MM; Dugan, LL; Behrens, MM; Lobner, D; Choi, DW
Citation
Neuroreport, 7(1):93-96, 1995
Journal Title
Neuroreport
ISSN
0959-49651473-558X
Abstract
Free radical-mediated damage to cultured cortical neurons was induced by a 24 h exposure to Fe2+ (30 microM) or an inhibitor of gamma-glutamylcysteine synthetase, L-buthionine-[S,R]-sulfoximine (BSO, 1 mM). As expected, neuronal death was blocked by inclusion of the free radical scavenger trolox during the Fe2+ or BSO exposure. However, unexpectedly, pretreatment of the cultures with BDNF or IGF-I markedly potentiated neuronal death. This growth factor-potentiated death was still blocked by trolox, but was insensitive to glutamate antagonists. Concurrent addition of cycloheximide with the growth factors prevented injury potentiation. Present findings suggest that growth factors may increase free radical-induced neuronal death by mechanisms dependent upon protein synthesis.
MeSH terms
AnimalsBrain-Derived Neurotrophic FactorButhionine SulfoximineCell Death/drug effectsCells, CulturedCerebral Cortex/*drug effects/pathologyDrug SynergismEnzyme Inhibitors/toxicityFerric Compounds/toxicityGlutamate-Cysteine Ligase/antagonists & inhibitorsInsulin-Like Growth Factor I/*pharmacologyMethionine Sulfoximine/analogs & derivatives/toxicityMiceNerve Growth Factors/*pharmacologyNerve Tissue Proteins/*pharmacologyNeurons/*drug effects/pathology
PMID
8742425
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
AJOU Authors
곽, 병주
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