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Ochratoxin A-induced cytotoxicity, genotoxicity and reactive oxygen species in kidney cells: an integrative approach of complementary endpoints

2015-12-02Journal article Restricted access
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dc.contributor.authorCosta, J.G.
dc.contributor.authorSaraiva, N.
dc.contributor.authorGuerreiro, P.S.
dc.contributor.authorLouro, Henriqueta
dc.contributor.authorSilva, Maria João
dc.contributor.authorMiranda, J.P.
dc.contributor.authorCastro, M.
dc.contributor.authorBatinic-Haberle, I.
dc.contributor.authorFernandes, A.S.
dc.contributor.authorOliveira, N.G.
dc.date.accessioned2016-02-18T17:29:15Z
dc.date.available2017-11-25T01:30:08Z
dc.date.issued2015-12-02
dc.description.abstractOchratoxin A (OTA) is a well-known nephrotoxic and potential carcinogenic agent but no consensus about the molecular mechanisms underlying its deleterious effects has been reached yet. The aim of this study is to integrate several endpoints concerning OTA-induced toxicological effects in Vero kidney cells in order to obtain additional mechanistic data, especially regarding the influence of reactive oxygen species (ROS). One innovative aspect of this work is the use of the superoxide dismutase mimic (SODm) MnTnHex-2-PyP as a mechanistic tool to clarify the involvement of oxidative stress in OTA toxicity. The results showed concentration and time-dependent cytotoxic effects of OTA (crystal violet, neutral red and LDH leakage assays). While the SODm mildly increased cell viability, trolox and ascorbic acid had no effect with regards to this endpoint. OTA induced micronuclei formation. Using the FPG modified comet assay, OTA modestly increased the % of DNA in tail, revealing the presence of oxidative DNA lesions. This mycotoxin increased apoptosis, which was attenuated by SODm. In addition, the SODm decreased the ROS accumulation observed in DHE assay. Taken together, our data suggest that ROS partially contribute to the cytotoxicity and genotoxicity of OTA, although other mechanisms may be relevant in OTA-induced deleterious effects.pt_PT
dc.description.sponsorshipThe current work was funded, in part, by iMed.ULisboa (UID/DTP/04138/2013), research grants SFRH/BPD/96719/2013 to JPM and SFRH/BD/70293/2010 to PSG from Fundação para a Ciência e a Tecnologia, Portugal, by European Cooperation in Science and Research (COST Action BM1203/EU-ROS) and by IBH general research funds.pt_PT
dc.identifier.citationFood Chem Toxicol. 2016 Jan;87:65-76. doi: 10.1016/j.fct.2015.11.018. Epub 2015 Dec 2pt_PT
dc.identifier.doi10.1016/j.fct.2015.11.018.pt_PT
dc.identifier.issn0278-6915
dc.identifier.urihttp://hdl.handle.net/10400.18/3430
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevier/ Pergamonpt_PT
dc.relation.publisherversionhttp://www.sciencedirect.com/science/article/pii/S0278691515301046pt_PT
dc.subjectGenotoxicidade Ambientalpt_PT
dc.subjectGenotoxicitypt_PT
dc.subjectOchratoxin Apt_PT
dc.subjectCytotoxicitypt_PT
dc.subjectReactive Oxygen Speciespt_PT
dc.subjectAntioxidantspt_PT
dc.subjectMnTnHex-2-PyPpt_PT
dc.titleOchratoxin A-induced cytotoxicity, genotoxicity and reactive oxygen species in kidney cells: an integrative approach of complementary endpointspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/UID%2FDTP%2F04138%2F2013/PT
oaire.citation.endPage76pt_PT
oaire.citation.startPage65pt_PT
oaire.citation.titleFood and Chemical Toxicologypt_PT
oaire.citation.volume87pt_PT
oaire.fundingStream5876
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsembargoedAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublication8b7dc2e1-c04d-4a11-8fa9-83ead9d8f256
relation.isProjectOfPublication.latestForDiscovery8b7dc2e1-c04d-4a11-8fa9-83ead9d8f256

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