A mechanism for zinc toxicity in neuroblastoma cells

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dc.contributor.authorDaniels W.M.U.
dc.contributor.authorHendricks J.
dc.contributor.authorSalie R.
dc.contributor.authorVan Rensburg S.J.
dc.date.accessioned2011-05-15T15:59:59Z
dc.date.available2011-05-15T15:59:59Z
dc.date.issued2004
dc.description.abstractZinc is an important component of proteins essential for normal functioning of the brain. However, it has been shown in vitro that this metal, at elevated levels, can be toxic to cells leading to their death. We investigated possible mechanisms of cell death caused by zinc: firstly, generation of reactive oxygen species, and secondly, the activation of the MAP-kinase pathway. Cell viability was assessed by means of the methyl-thiazolyl tetrazolium salt (MTT) assay and confirmed by tetramethylrhodamine methyl ester (TMRM) staining. We measured the phosphorylation status of Erk and p38 as indicators of MAP-kinase activity, using Western Blot techniques. A time curve was established when neuroblastoma (N2α) cells were exposed to 100 μM of zinc for 4, 12, and 24 h. Zinc caused a significant reduction in cell viability as early as 4 h, and indirectly stimulated the accumulation of reactive oxygen species as determined by 2.7 dichlorodihydrofluorescein diacetate (DCDHF) staining and confocal microscopy. Investigation of the MAP-kinase pathway indicated that Erk was downregulated, while p38 was stimulated. Our results therefore led us to conclude that in vitro, zinc toxicity involved the generation of reactive oxygen species and the activation of the MAP-kinase pathway.
dc.description.versionConference Paper
dc.identifier.citationMetabolic Brain Disease
dc.identifier.citation19
dc.identifier.citation02-Jan
dc.identifier.issn8857490
dc.identifier.other10.1023/B:MEBR.0000027419.79032.bd
dc.identifier.urihttp://hdl.handle.net/10019.1/11465
dc.subjectester derivative
dc.subjectfluorescein diacetate
dc.subjectmitogen activated protein kinase
dc.subjectmitogen activated protein kinase p38
dc.subjectreactive oxygen metabolite
dc.subjectrhodamine
dc.subjecttetrazolium
dc.subjectzinc
dc.subjectanimal cell
dc.subjectcell death
dc.subjectcell viability
dc.subjectconference paper
dc.subjectconfocal microscopy
dc.subjectcontrolled study
dc.subjectdown regulation
dc.subjectenzyme activation
dc.subjectenzyme activity
dc.subjectenzyme phosphorylation
dc.subjectneuroblastoma cell
dc.subjectnonhuman
dc.subjectrat
dc.subjectstaining
dc.subjectstatistical significance
dc.subjectWestern blotting
dc.subjectanimal
dc.subjectarticle
dc.subjectcell survival
dc.subjectcytology
dc.subjectdrug effect
dc.subjecthuman
dc.subjectmetabolism
dc.subjectnerve cell
dc.subjectneuroblastoma
dc.subjectphosphorylation
dc.subjectsignal transduction
dc.subjecttumor cell line
dc.subjectAnimalia
dc.subjectAnimals
dc.subjectCell Line, Tumor
dc.subjectCell Survival
dc.subjectHumans
dc.subjectMAP Kinase Signaling System
dc.subjectMitogen-Activated Protein Kinases
dc.subjectNeuroblastoma
dc.subjectNeurons
dc.subjectp38 Mitogen-Activated Protein Kinases
dc.subjectPhosphorylation
dc.subjectReactive Oxygen Species
dc.subjectZinc
dc.titleA mechanism for zinc toxicity in neuroblastoma cells
dc.typeConference Paper
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