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dc.contributor.authorYirun, Anil
dc.contributor.authorOzkemahli, Gizem
dc.contributor.authorBalci, Aylin
dc.contributor.authorErkekoglu, Pinar
dc.contributor.authorZeybek, Naciye Dilara
dc.contributor.authorYersal, Nilgun
dc.contributor.authorKocer-Gumusel, Belma
dc.date.accessioned2021-06-11T07:40:35Z
dc.date.available2021-06-11T07:40:35Z
dc.date.issued2021-06-01
dc.identifier.other33496947
dc.identifier.urihttp://hdl.handle.net/20.500.12591/577
dc.description.abstractBisphenol A (BPA) and di(2-ethylhexyl)phthalate (DEHP) are abundant endocrine disrupting chemicals (EDCs). In recent years, studies showed that EDCs may lead to neurodevelopmental diseases. The effects of prenatal exposure to these chemicals may have serious consequences. Moreover, exposure to EDCs as a mixture may have different effects than individual exposures. The present study aimed to determine the toxicity of BPA and/or DEHP on central nervous system (CNS) and neuroendocrine system in prenatal and lactational period in Sprague-Dawley rats. Pregnant rats were randomly divided into four groups: control (received vehicle); BPA group (received BPA at 50 mg/kg/day); DEHP group (received DEHP at 30 mg/kg/day); and combined exposure group (received both BPA at 50 mg/kg/day and DEHP at 30 mg/kg/day) during pregnancy and lactation by oral gavage. At the end of lactation, male offspring (n = 6) were randomly grouped. The alterations in the brain histopathology, neurotransmitter levels and enzyme activities in the cerebrum region, oxidative stress markers, and apoptotic effects in the hippocampus region were determined at adulthood. The results showed that exposure to EDCs at early stages of life caused significant changes in lipid peroxidation, total GSH and neurotransmitter levels, and activities of neurotransmitter-related enzymes. Moreover, BPA and/or DEHP led to apoptosis and histopathologic alterations in the hippocampus. Therefore, we can suggest that changes in oxidant/antioxidant status, as well as in neurotransmitters and related enzymes, can be considered as the underlying neurotoxicity mechanisms of BPA and DEHP. However, more mechanistic studies are needed.en_US
dc.language.isoengen_US
dc.publisherEzcacılık Fakültesien_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
dc.subjectApoptosisen_US
dc.subjectBisphenol Aen_US
dc.subjectDi(2-ethylhexyl) phthalateen_US
dc.subjectEndocrine disrupting chemicalsen_US
dc.subjectLactational exposureen_US
dc.subjectNeurotoxicityen_US
dc.subjectOxidative stressen_US
dc.subjectPrenatal exposureen_US
dc.titleNeuroendocrine disruption by bisphenol A and/or di(2-ethylhexyl) phthalate after prenatal, early postnatal and lactational exposure.en_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.contributor.departmentFarmasötik Toksikolojien_US


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