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Zn2+ entry produces oxidative neuronal necrosis in cortical cell cultures.

DC Field Value Language
dc.contributor.authorKim, EY-
dc.contributor.authorKoh, JY-
dc.contributor.authorKim, YH-
dc.contributor.authorSohn, S-
dc.contributor.authorJoe, E-
dc.contributor.authorGwag, BJ-
dc.date.accessioned2011-09-06-
dc.date.available2011-09-06-
dc.date.issued1999-
dc.identifier.issn0953-816X-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/4025-
dc.description.abstractEvidence has accumulated that Zn2+ plays a central role in neurodegenerative processes following brain injuries including ischaemia or epilepsy. In the present study, we examined patterns and possible mechanisms of Zn2+ neurotoxicity. Inclusion of 30-300 microM Zn2+ for 30 min caused neuronal necrosis apparent by cell body and mitochondrial swelling in cortical cell cultures. This Zn2+ neurotoxicity was not attenuated by antiapoptosis agents, inhibitors of protein synthesis or caspase. Blockade of glutamate receptors or nitric oxide synthase showed no beneficial effect against Zn2+ neurotoxicity. Interestingly, antioxidants, trolox or SKF38393, attenuated Zn(2+)-induced neuronal necrosis. Pretreatment with insulin or brain-derived neurotrophic factor increased the Zn(2+)-induced free radical injury. Kainate or AMPA facilitated Zn2+ entry and potentiated Zn2+ neurotoxicity in a way sensitive to trolox. Reactive oxygen species and lipid peroxidation were generated in the early phase of Zn2+ neurotoxicity. These findings indicate that entry and accumulation of Zn2+ result in generation of toxic free radicals and then cause necrotic neuronal degeneration under certain pathological conditions in the brain.-
dc.language.isoen-
dc.subject.MESH2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine-
dc.subject.MESH6-Cyano-7-nitroquinoxaline-2,3-dione-
dc.subject.MESHAmino Acid Chloromethyl Ketones-
dc.subject.MESHAnimals-
dc.subject.MESHAntioxidants-
dc.subject.MESHApoptosis-
dc.subject.MESHBrain-Derived Neurotrophic Factor-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCerebral Cortex-
dc.subject.MESHChromans-
dc.subject.MESHCysteine Proteinase Inhibitors-
dc.subject.MESHDizocilpine Maleate-
dc.subject.MESHDopamine Agonists-
dc.subject.MESHDrug Synergism-
dc.subject.MESHExcitatory Amino Acid Agonists-
dc.subject.MESHExcitatory Amino Acid Antagonists-
dc.subject.MESHFemale-
dc.subject.MESHFree Radicals-
dc.subject.MESHHypoglycemic Agents-
dc.subject.MESHInsulin-
dc.subject.MESHKainic Acid-
dc.subject.MESHLipid Peroxidation-
dc.subject.MESHMice-
dc.subject.MESHMicroscopy, Electron-
dc.subject.MESHMitochondrial Swelling-
dc.subject.MESHNecrosis-
dc.subject.MESHNerve Degeneration-
dc.subject.MESHNeurons-
dc.subject.MESHNeurotoxins-
dc.subject.MESHOligopeptides-
dc.subject.MESHOxidative Stress-
dc.subject.MESHPregnancy-
dc.subject.MESHZinc-
dc.subject.MESHalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid-
dc.titleZn2+ entry produces oxidative neuronal necrosis in cortical cell cultures.-
dc.typeArticle-
dc.identifier.pmid9987035-
dc.identifier.urlhttp://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0953-816X&date=1999&volume=11&issue=1&spage=327-
dc.contributor.affiliatedAuthor손, 성향-
dc.contributor.affiliatedAuthor조, 은혜-
dc.contributor.affiliatedAuthor곽, 병주-
dc.type.localJournal Papers-
dc.citation.titleThe European journal of neuroscience-
dc.citation.volume11-
dc.citation.number1-
dc.citation.date1999-
dc.citation.startPage327-
dc.citation.endPage334-
dc.identifier.bibliographicCitationThe European journal of neuroscience, 11(1). : 327-334, 1999-
dc.identifier.eissn1460-9568-
dc.relation.journalidJ00953816X-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
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