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Cobalt chloride speciation, mechanisms of cytotoxicity on human pulmonary cells, and synergistic toxicity with zinc

hal.structure.identifierLaboratoire de Spéciation des Radionucléides et des Molécules [LSRM]
dc.contributor.authorBRESSON, C.
dc.contributor.authorDAROLLES, C.
hal.structure.identifierInterface Physique et Chimie pour le Vivant [IPCV]
dc.contributor.authorCARMONA, A.
dc.contributor.authorGAUTIER, Christian
dc.contributor.authorSAGE, N.
hal.structure.identifierInterface Physique et Chimie pour le Vivant [IPCV]
dc.contributor.authorROUDEAU, S.
hal.structure.identifierInterface Physique et Chimie pour le Vivant [IPCV]
dc.contributor.authorORTEGA, R.
dc.contributor.authorANSOBORLOF, E.
dc.contributor.authorMALARDB, V.
dc.date.issued2013
dc.identifier.issn1756-5901
dc.description.abstractEnCobalt is used in numerous industrial sectors, leading to occupational diseases, particularly by inhalation. Cobalt-associated mechanisms of toxicity are far from being understood and information that could improve knowledge in this area is required. We investigated the impact of a soluble cobalt compound, CoCl2*6H2O, on the BEAS-2B lung epithelial cell line, as well as its impact on metal homeostasis. Cobalt speciation in different culture media, in particular soluble and precipitated cobalt species, was investigated via theoretical and analytical approaches. The cytotoxic effects of cobalt on the cells were assessed. Upon exposure of BEAS-2B cells to cobalt, intracellular accumulation of cobalt and zinc was demonstrated using direct in situ microchemical analysis based on ion micro-beam techniques and analysis after cell lysis by inductively coupled plasma mass spectrometry (ICP-MS). Microchemical imaging revealed that cobalt was rather homogeneously distributed in the nucleus and in the cytoplasm whereas zinc was more abundant in the nucleus. The modulation of zinc homeostasis led to the evaluation of the effect of combined cobalt and zinc exposure. In this case, a clear synergistic increase in toxicity was observed as well as a substantial increase in zinc content within cells. Western blots performed under the same coexposure conditions revealed a decrease in ZnT1 expression, suggesting that cobalt could inhibit zinc release through the modulation of ZnT1. Overall, this study highlights the potential hazard to lung function, of combined exposure to cobalt and zinc.
dc.language.isoen
dc.publisherRoyal Society of Chemistry
dc.title.enCobalt chloride speciation, mechanisms of cytotoxicity on human pulmonary cells, and synergistic toxicity with zinc
dc.typeArticle de revue
dc.identifier.doi10.1039/C3MT20196A
dc.subject.halSciences du Vivant [q-bio]/Toxicologie
bordeaux.journalMetallomics
bordeaux.page133-143
bordeaux.volume5
bordeaux.peerReviewedoui
hal.identifierin2p3-00823540
hal.version1
hal.popularnon
hal.audienceNon spécifiée
hal.origin.linkhttps://hal.archives-ouvertes.fr//in2p3-00823540v1
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