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Cytotoxicity measurement of Bisphenol A (BPA) and its substitutes using human keratinocytes

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dc.contributor.authorSon, Seogho-
dc.contributor.authorNam, KeeSoo-
dc.contributor.authorKim, Hyungjoo-
dc.contributor.authorGye, Myung Chan-
dc.contributor.authorShin, Incheol-
dc.date.accessioned2021-08-02T13:27:18Z-
dc.date.available2021-08-02T13:27:18Z-
dc.date.created2021-05-12-
dc.date.issued2018-07-
dc.identifier.issn0013-9351-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/16820-
dc.description.abstractBisphenol-A (BPA) was first synthesized in the 1890s and has been used in many plastic products. However, BPA is known to act as an endocrine disruptor and has been found to be toxic to human health. Many alternative substances have been developed to replace BPA, but it is still widely used worldwide. In this study, we identified the potential cytotoxicity of BPA by evaluating toxicity using human keratinocytes. Also, we evaluated cytotoxicity of BPA substitutes to determine their suitability as an alternative to BPA. The proliferation assay using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry and western blot analysis showed that BPA significantly affect cell viability, induction of apoptotic fraction and increased activation of DNA-damage marker protein. In addition, through the same experiments, the substitutes of BPA were shown to be significantly less toxic than BPA, and the least toxicity was observed with 1,4-cyclohexanedimethanol (CHDM) and terephthalic acid (TPA). In conclusion, this study suggests that cytotoxicity of BPA induces apoptosis of human keratinocytes, and that CHDM and TPA are the most suitable substitutes for BPA.-
dc.language영어-
dc.language.isoen-
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE-
dc.titleCytotoxicity measurement of Bisphenol A (BPA) and its substitutes using human keratinocytes-
dc.typeArticle-
dc.contributor.affiliatedAuthorGye, Myung Chan-
dc.contributor.affiliatedAuthorShin, Incheol-
dc.identifier.doi10.1016/j.envres.2018.03.043-
dc.identifier.scopusid2-s2.0-85045016624-
dc.identifier.wosid000431387100075-
dc.identifier.bibliographicCitationENVIRONMENTAL RESEARCH, v.164, pp.655 - 659-
dc.relation.isPartOfENVIRONMENTAL RESEARCH-
dc.citation.titleENVIRONMENTAL RESEARCH-
dc.citation.volume164-
dc.citation.startPage655-
dc.citation.endPage659-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaEnvironmental Sciences & Ecology-
dc.relation.journalResearchAreaPublic, Environmental & Occupational Health-
dc.relation.journalWebOfScienceCategoryEnvironmental Sciences-
dc.relation.journalWebOfScienceCategoryPublic, Environmental & Occupational Health-
dc.subject.keywordPlusWIDESPREAD EXPOSURE-
dc.subject.keywordPlusHUMAN HEALTH-
dc.subject.keywordPlusESTROGENICITY-
dc.subject.keywordPlusCHEMICALS-
dc.subject.keywordAuthorApoptosis-
dc.subject.keywordAuthorBisphenol A-
dc.subject.keywordAuthorBPA substitutes-
dc.subject.keywordAuthorEndocrine disruptor-
dc.subject.keywordAuthorHaCaT-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0013935118301750?via%3Dihub-
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