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Cytotoxic and Genotoxic Effects of Environmental Relevant Concentrations of Bisphenol A and Interactions with Doxorubicin

2019Journal article Open access
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dc.contributor.authorRamos, C
dc.contributor.authorLadeira, C
dc.contributor.authorZeferino, S
dc.contributor.authorDias, A
dc.contributor.authorFaria, I
dc.contributor.authorCristovam, E
dc.contributor.authorGomes, M
dc.contributor.authorRibeiro, E
dc.date.accessioned2024-04-12T15:40:49Z
dc.date.available2024-04-12T15:40:49Z
dc.date.issued2019
dc.description.abstractBisphenol A (BPA) is one of the most widely utilized endocrine disruptors to which humans are exposed, particularity through ingestion. BPA is an aneugenic compound with a putative association to tumorigenesis. Although extensively studied in estrogen responsive cells, information regarding its effects on cells from the upper gastrointestinal tract exposed to free/active forms of BPA is still scarce. Similarly, BPA interactions with other drugs have been neglected, although it has been suggested to have a potential role in doxorubicin (DOX) chemoresistance. This study is intended to assess potential cytotoxic and genotoxic effects of BPA, as well as its interactions with DOX, in Human epithelial type 2 cells (Hep-2) originated from a human laryngeal carcinoma and in a DNA damage responsive cell line, the human lung fibroblasts (MRC-5). Cell viability was analyzed through the resazurin assay. The G protein-coupled estrogen receptor 1 (GPER) expression was visualized by immunodetection. Genotoxicity, namely DNA damage and oxidative DNA damage, were assessed by comet assay and micronuclei induction, and mitotic disruption was evaluated cytologically by fluorescent microscopy with DAPI staining. Cytotoxicity analysis showed that exposure to BPA per se does not affect cellular viability. Nevertheless, the genotoxic analysis showed that BPA induced an increase of DNA damage in the Hep-2 cell line and in oxidative damage in the MRC-5 cell line. An increase of micronuclei was also observed in both cell lines following BPA exposure. BPA and DOX co-exposures suggested that BPA acts as an antagonist of DOX effects in both cell lines. The interaction with DOX appears to be cell type dependent, exhibiting a non-monotonic response curve in MRC-5 cells, a GPER expressing cell line. Our study emphasizes the need for a deeper knowledge of BPA interactions, particularly with chemotherapeutic agents, in the context of risk assessment and public health.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationMutat Res Genet Toxicol Environ Mutagen . 2019 Feb:838:28-36.pt_PT
dc.identifier.doi10.1016/j.mrgentox.2018.11.009pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.17/4877
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.subjectCHLC PAT CLINpt_PT
dc.subjectBenzhydryl Compounds / toxicity*pt_PT
dc.subjectHumanspt_PT
dc.subjectCell Line, Tumorpt_PT
dc.subjectCell Transformation, Neoplastic / chemically induced*pt_PT
dc.subjectComet Assaypt_PT
dc.subjectDNA Damage / drug effects*pt_PT
dc.subjectDoxorubicin / pharmacology*pt_PT
dc.subjectDrug Interactions / physiologypt_PT
dc.subjectEndocrine Disruptors / toxicity*pt_PT
dc.subjectMicronucleus Testspt_PT
dc.subjectPhenols / toxicity*pt_PT
dc.subjectReceptors, Estrogen / biosynthesispt_PT
dc.subjectReceptors, G-Protein-Coupled / biosynthesispt_PT
dc.titleCytotoxic and Genotoxic Effects of Environmental Relevant Concentrations of Bisphenol A and Interactions with Doxorubicinpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage36pt_PT
oaire.citation.startPage28pt_PT
oaire.citation.titleMutation Research/Genetic Toxicology and Environmental Mutagenesispt_PT
oaire.citation.volume838pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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