Phenotypic anchoring of arsenic and cadmium toxicity in three hepatic-related cell systems reveals compound- and cell-specific selective up-regulation of stress protein expression: Implications for fingerprint profiling of cytotoxicity

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dc.contributor.authorGottschalg, Elke
dc.contributor.authorMoore, Nicholas E.
dc.contributor.authorRyan, Abigail K.
dc.contributor.authorTravis, Lucy C.
dc.contributor.authorWaller, Ruth C.
dc.contributor.authorPratt, Steven
dc.contributor.authorAtmaca, Mukadder
dc.date.accessioned2024-04-24T16:11:00Z
dc.date.available2024-04-24T16:11:00Z
dc.date.issued2006
dc.departmentDicle Üniversitesien_US
dc.description.abstractExposure of cells to toxic chemicals is known to up-regulate the expression of a number of stress proteins (SPs), including metallothionein (MT) and members of the heat shock protein (HSP) family, and this response may allow the development of a fingerprint profile to identify mechanisms of toxicity in an in vitro toxicology setting. To test this hypothesis, three hepatic-derived cell culture systems (rat hepatoma FGC4 cell line, rat hepatocytes, human hepatoma HepG2 cell line) were exposed to cadmium (as CdCl2) and arsenic (as NaASO(2)), two compounds believed to exert their toxicity through an oxidative stress mechanism, under conditions of phenotypic anchoring defined as minimal and mild toxicity (approximately 5 and 25% reduction in neutral red uptake, respectively). The expression of six SPs - MT, HSP25/27, HSP40, HSP60, HSP70, and HSP90 - was then determined by ELISA. Expression of four of these SPs - MT, HSP25/27, HSP40 and HSP70 - was up-regulated in at least one experimental condition. However, the patterns of expression of these four SPs varied across the experimental conditions, according to differences in toxicant concentration and/or level of toxicity, cell-type and toxicant itself. This lack of uniformity in response of a focussed set of mechanistically defensible targets suggests that similar problems may emerge when using more global approaches based on genomics and proteomics, in which problems of redundancy in targets and uncertain mechanistic relevance will be greater. (c) 2006 Elsevier Ireland Ltd. All rights reserved.en_US
dc.identifier.doi10.1016/j.cbi.2006.04.003
dc.identifier.endpage261en_US
dc.identifier.issn0009-2797
dc.identifier.issue3en_US
dc.identifier.pmid16729991
dc.identifier.scopus2-s2.0-33746260458
dc.identifier.scopusqualityQ1
dc.identifier.startpage251en_US
dc.identifier.urihttps://doi.org/10.1016/j.cbi.2006.04.003
dc.identifier.urihttps://hdl.handle.net/11468/15226
dc.identifier.volume161en_US
dc.identifier.wosWOS:000239982200092
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherElsevier Ireland Ltden_US
dc.relation.ispartofChemico-Biological Interactions
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCytotoxicityen_US
dc.subjectStress Proteinsen_US
dc.subjectMetallothioneinen_US
dc.subjectHeat Shock Proteinsen_US
dc.subjectCadmiumen_US
dc.subjectArsenicen_US
dc.subjectPhenotypic Anchoringen_US
dc.subjectFgc4 Cellsen_US
dc.subjectRat Hepatocytesen_US
dc.subjectHepg2 Cellsen_US
dc.titlePhenotypic anchoring of arsenic and cadmium toxicity in three hepatic-related cell systems reveals compound- and cell-specific selective up-regulation of stress protein expression: Implications for fingerprint profiling of cytotoxicityen_US
dc.titlePhenotypic anchoring of arsenic and cadmium toxicity in three hepatic-related cell systems reveals compound- and cell-specific selective up-regulation of stress protein expression: Implications for fingerprint profiling of cytotoxicity
dc.typeArticleen_US

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