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Assessment of oxidative damage induced by iron oxide nanoparticles on different nervous system cells

2018-11-30Journal article Restricted access
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dc.contributor.authorFernández-Bertólez, Natalia
dc.contributor.authorCosta, Carla
dc.contributor.authorBessa, Maria João
dc.contributor.authorPark, Magriet
dc.contributor.authorCarriere, Marie
dc.contributor.authorDussert, Fanny
dc.contributor.authorTeixeira, João Paulo
dc.contributor.authorPásaro, Eduardo
dc.contributor.authorLaffon, Blanca
dc.contributor.authorValdiglesias, Vanessa
dc.date.accessioned2019-03-06T15:36:14Z
dc.date.available2019-03-06T15:36:14Z
dc.date.issued2018-11-30
dc.description.abstractIron oxide nanoparticles (ION) have received much attention for their utility in biomedical applications, such as magnetic resonance imaging, drug delivery and hyperthermia, but concerns regarding their potential harmful effects are also growing. Even though ION may induce different toxic effects in a wide variety of cell types and animal systems, there is a notable lack of toxicological data on the human nervous system, particularly important given the increasing number of applications on this specific system. An important mechanism of nanotoxicity is reactive oxygen species (ROS) generation and oxidative stress. On this basis, the main objective of this work was to assess the oxidative potential of silica-coated (S-ION) and oleic acid-coated (O-ION) ION on human SH-SY5Y neuronal and A172 glial cells. To this aim, ability of ION to generate ROS (both in the absence and presence of cells) was determined, and consequences of oxidative potential were assessed (i) on DNA by means of the 8-oxo-7,8-dihydroguanine DNA glycosylase (OGG1)-modified comet assay, and (ii) on antioxidant reserves by analyzing ratio of reduced glutathione (GSH) to oxidized glutathione (GSSG). Conditions tested included a range of concentrations, two exposure times (3 and 24 h), and absence and presence of serum in the cell culture media. Results confirmed that, even though ION were not able to produce ROS in acellular environments, ROS formation was increased in the neuronal and glial cells by ION exposure, and was parallel to induction of oxidative DNA damage and, only in the case of neuronal cells treated with S-ION, to decreases in the GSH/GSSG ratio. Present findings suggest the production of oxidative stress as a potential action mechanism leading to the previously reported cellular effects, and indicate that ION may pose a health risk to human nervous system cells by generating oxidative stress, and thus should be used with caution.pt_PT
dc.description.sponsorshipThis work was funded by Xunta de Galicia (ED431B 2016/013). V. Valdiglesias was supported by a Xunta de Galicia postdoctoral fellowship (reference ED481B 2016/190-0). N. Fernández-Bertólez was supported by an INDITEX-UDC fellowship, and Maria João Bessa was supported by the grant SFRH/BD/120646/2016, funded by FCT (financing subsided by national fund of MCTES and POCH). Authors would also like to acknowledge COST Action CA15132 “The comet assay as a human biomonitoring tool (hCOMET)”.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationMutat Res Gen Tox En. 2018 Nov 30:1-10. doi: 10.1016/j.mrgentox.2018.11.013pt_PT
dc.identifier.doi10.1016/j.mrgentox.2018.11.013pt_PT
dc.identifier.issn1383-5718
dc.identifier.urihttp://hdl.handle.net/10400.18/6074
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S1383571818302717
dc.subjectIron Oxide Nanoparticlespt_PT
dc.subjectOxidative DNA Damagept_PT
dc.subjectReactive Oxygen Speciespt_PT
dc.subjectGlutathione Depletionpt_PT
dc.subjectSH-SY5Y Cellspt_PT
dc.subjectA172 Cellspt_PT
dc.subjectGenotoxicidade Ambientalpt_PT
dc.titleAssessment of oxidative damage induced by iron oxide nanoparticles on different nervous system cellspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage10pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleMutation Research - Genetic Toxicology and Environmental Mutagenesispt_PT
rcaap.rightsembargoedAccesspt_PT
rcaap.typearticlept_PT

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