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dc.contributor.authorErkekoglu, P.en_US
dc.contributor.authorRachidi, W.en_US
dc.contributor.authorYuzugullu, O. G.en_US
dc.contributor.authorGiray, B.en_US
dc.contributor.authorFavier, A.en_US
dc.contributor.authorOzturk, M.en_US
dc.contributor.authorHincal, F.en_US
dc.date.accessioned2016-02-08T09:56:39Z
dc.date.available2016-02-08T09:56:39Z
dc.date.issued2010en_US
dc.identifier.issn0041-008X
dc.identifier.urihttp://hdl.handle.net/11693/22186
dc.description.abstractDi(2-ethylhexyl)-phthalate (DEHP) is the most abundantly used phthalate derivative, inevitable environmental exposure of which is suspected to contribute to the increasing incidence of testicular dysgenesis syndrome in humans. Oxidative stress and mitochondrial dysfunction in germ cells are suggested to contribute to phthalate-induced disruption of spermatogenesis in rodents, and Leydig cells are one of the main targets of phthalates' testicular toxicity. Selenium is known to be involved in the modulation of intracellular redox equilibrium, and plays a critical role in testis, sperm, and reproduction. This study was aimed to investigate the oxidative stress potential of DEHP and its consequences in testicular cells, and examine the possible protective effects of selenium using the MA-10 mouse Leydig tumor cell line as a model. In the presence and absence of selenium compounds [30. nM sodium selenite (SS), and 10 μM selenomethionine (SM)], the effects of exposure to DEHP and its main metabolite mono(2-ethylhexyl)-phthalate (MEHP) on the cell viability, enzymatic and non-enzymatic antioxidant status, ROS production, p53 expression, and DNA damage by alkaline Comet assay were investigated. The overall results of this study demonstrated the cytotoxicity and genotoxicity potential of DEHP, where MEHP was found to be more potent than the parent compound. SS and SM produced almost the same level of protection against antioxidant status modifying effects, ROS and p53 inducing potentials, and DNA damaging effects of the two phthalate derivatives. It was thus shown that DEHP produced oxidative stress in MA-10 cells, and selenium supplementation appeared to be an effective redox regulator in the experimental conditions used in this study, emphasizing the critical importance of the appropriate selenium status. © 2010 Elsevier Inc.en_US
dc.language.isoEnglishen_US
dc.source.titleToxicology and Applied Pharmacologyen_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/j.taap.2010.07.016en_US
dc.subjectAntioxidant enzymesen_US
dc.subjectComet assayen_US
dc.subjectCytotoxicityen_US
dc.subjectDi(2-ethylhexyl)-phthalateen_US
dc.subjectMono(2-ethylhexyl)-phthalateen_US
dc.subjectOxidative stressen_US
dc.subjectP53en_US
dc.subjectSeleniumen_US
dc.subjectCell DNAen_US
dc.titleEvaluation of cytotoxicity and oxidative DNA damaging effects of di(2-ethylhexyl)-phthalate (DEHP) and mono(2-ethylhexyl)-phthalate (MEHP) on MA-10 Leydig cells and protection by seleniumen_US
dc.typeArticleen_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.citation.spage52en_US
dc.citation.epage62en_US
dc.citation.volumeNumber248en_US
dc.citation.issueNumber1en_US
dc.identifier.doi10.1016/j.taap.2010.07.016en_US
dc.publisherElsevieren_US


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