Induction of ROS, p53, p21 in DEHP-and MEHP-exposed LNCaP cells-protection by selenium compunds

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dc.citation.epage1571en_US
dc.citation.issueNumber7en_US
dc.citation.spage1565en_US
dc.citation.volumeNumber49en_US
dc.contributor.authorErkekoglu, P.en_US
dc.contributor.authorRachidi, W.en_US
dc.contributor.authorYazgullu, O. G.en_US
dc.contributor.authorGiray, B.en_US
dc.contributor.authorOzturk, M.en_US
dc.contributor.authorFavier, A.en_US
dc.contributor.authorHincal, F.en_US
dc.date.accessioned2015-07-28T12:00:18Z
dc.date.available2015-07-28T12:00:18Z
dc.date.issued2011-07en_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.description.abstractThis study was designed to investigate the hypothesis that the toxic effects of di(2-ethylhexyl)phthalate (DEHP), the most abundantly used plasticizer and ubiquitous environmental contaminant that cause alterations in endocrine and spermatogenic functions in animals is mediated through the induction of reactive oxygen species (ROS) and activation of nuclear p53 and p21 proteins in LNCaP human prostate adenocarcinoma cell line. Protective effects of two selenocompounds, sodium selenite (SS) and selenomethionine (SM) were also examined. It was demonstrated that 24. h exposure of the cells to 3. mM DEHP or its main metabolite, mono(2-ethylhexyl)phthalate (MEHP, 3 μM) caused strongly amplified production of ROS. Both SS (30. nM) and SM (10 μM) supplementations reduced ROS production, and p53 and p21 activation that induced significantly only by MEHP-exposure. The overall results of this study indicated that the induction of oxidative stress is one of the important mechanisms underlying the toxicity of DEHP and this is mainly through the effects of the metabolite, MEHP. Generated data also emphasized the critical role of Se in modulation of intracellular redox status, implicating the importance of the appropriate Se status in cellular response against testicular toxicity of phthalates. © 2011 Elsevier Ltd.en_US
dc.identifier.doi10.1016/j.fct.2011.04.001en_US
dc.identifier.issn0278-6915
dc.identifier.urihttp://hdl.handle.net/11693/12159
dc.language.isoEnglishen_US
dc.publisherElsevieren_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.fct.2011.04.001en_US
dc.source.titleFood and Chemical Toxicologyen_US
dc.subjectDehpen_US
dc.subjectMehpen_US
dc.subjectP53en_US
dc.subjectP21en_US
dc.subjectRosen_US
dc.subjectSeleniumen_US
dc.subjectOxidative Stressen_US
dc.subjectDi(2-ethylhexyl) Phthalateen_US
dc.subjectDna-damageen_US
dc.subjectPeroxisome Proliferatorsen_US
dc.subjectDiethylhexyl Phthalateen_US
dc.subjectCancer Preventionen_US
dc.subjectGene-expressionen_US
dc.subjectIn-vitroen_US
dc.subjectApoptosisen_US
dc.subjectMechanismsen_US
dc.titleInduction of ROS, p53, p21 in DEHP-and MEHP-exposed LNCaP cells-protection by selenium compundsen_US
dc.typeArticleen_US

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