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Analysis of the activation routes induced by different metal oxide nanoparticles on human lung epithelial cells.

ABSTRACT: Nanoparticles (Nps) can induce toxicity in the lung by accidental or intentional exposure. The main objective of the study reported here was to characterize the effect that four metal oxide Nps (CeO₂, TiO₂, Al₂O₃ and ZnO) had at the cellular level on a human lung epithelial cell line. This goal was achieved by studying the capacity of the Nps to activate the main mitogen-activated protein kinases (MAPKs) and the nuclear factor NFκB. Only ZnO Nps were able to activate all of the MAPKs and the release of Zn²⁺ ions was the main cause of activation. ZnO and Al₂O₃ Nps activated the NFκB pathway and induced the release of inflammatory cytokines. CeO₂ and TiO₂ Nps were found to have safer profiles. The graphical abstract was obtained using Servier Medical Art.

SUBMITTER: Simon-Vazquez R

PROVIDER: S-EPMC5137956 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature

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Analysis of the activation routes induced by different metal oxide nanoparticles on human lung epithelial cells.

Simón-Vázquez Rosana R Lozano-Fernández Tamara T Dávila-Grana Angela A González-Fernández África Á

Future science OA 20160415 2

Nanoparticles (Nps) can induce toxicity in the lung by accidental or intentional exposure. The main objective of the study reported here was to characterize the effect that four metal oxide Nps (CeO2, TiO2, Al2O3 and ZnO) had at the cellular level on a human lung epithelial cell line. This goal was achieved by studying the capacity of the Nps to activate the main mitogen-activated protein kinases (MAPKs) and the nuclear factor NFκB. Only ZnO Nps were a ...[more]

PMID: 28031965

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Project description:BackgroundGenotoxicity is an important toxicological endpoint due to the link to diseases such as cancer. Therefore, an increased understanding regarding genotoxicity and underlying mechanisms is needed for assessing the risk with exposure to nanoparticles (NPs). The aim of this study was to perform an in-depth investigation regarding the genotoxicity of well-characterized Ni and NiO NPs in human bronchial epithelial BEAS-2B cells and to discern possible mechanisms. Comparisons were made with NiCl2 in order to elucidate effects of ionic Ni.MethodsBEAS-2B cells were exposed to Ni and NiO NPs, as well as NiCl2, and uptake and cellular dose were investigated by transmission electron microscopy (TEM) and inductively coupled plasma mass spectrometry (ICP-MS). The NPs were characterized in terms of surface composition (X-ray photoelectron spectroscopy), agglomeration (photon cross correlation spectroscopy) and nickel release in cell medium (ICP-MS). Cell death (necrosis/apoptosis) was investigated by Annexin V-FITC/PI staining and genotoxicity by cytokinesis-block micronucleus (cytome) assay (OECD 487), chromosomal aberration (OECD 473) and comet assay. The involvement of intracellular reactive oxygen species (ROS) and calcium was explored using the fluorescent probes, DCFH-DA and Fluo-4.ResultsNPs were efficiently taken up by the BEAS-2B cells. In contrast, no or minor uptake was observed for ionic Ni from NiCl2. Despite differences in uptake, all exposures (NiO, Ni NPs and NiCl2) caused chromosomal damage. Furthermore, NiO NPs were most potent in causing DNA strand breaks and generating intracellular ROS. An increase in intracellular calcium was observed and modulation of intracellular calcium by using inhibitors and chelators clearly prevented the chromosomal damage. Chelation of iron also protected against induced damage, particularly for NiO and NiCl2.ConclusionsThis study has revealed chromosomal damage by Ni and NiO NPs as well as Ni ionic species and provides novel evidence for a calcium-dependent mechanism of cyto- and genotoxicity.

Dataset Information

Analysis of the activation routes induced by different metal oxide nanoparticles on human lung epithelial cells.

Publications

Analysis of the activation routes induced by different metal oxide nanoparticles on human lung epithelial cells.

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