Acrylamide applied during pregnancy causes the neurotoxic effect by lowering BDNF levels in the fetal brain

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dc.authoridGozukara Bag, Harika Gozde/0000-0003-1208-4072
dc.authoridAltinoz, Eyup/0000-0002-3991-9773
dc.contributor.authorErdemli, Mehmet Erman
dc.contributor.authorAladag, M. Arif
dc.contributor.authorAltinoz, Eyup
dc.contributor.authorDemirtas, Sezin
dc.contributor.authorTurkoz, Yusuf
dc.contributor.authorYigitcan, Birgul
dc.contributor.authorBag, Harika Gozukara
dc.date.accessioned2024-11-07T13:34:23Z
dc.date.available2024-11-07T13:34:23Z
dc.date.issued2018
dc.departmentNiğde Ömer Halisdemir Üniversitesi
dc.description.abstractObjectives: The aim of this study is to elucidate the possible mechanism of neurotoxic effect of acrylamide (AA) applied during pregnancy on fetal brain development and to show the effect of N-acetylcysteine (NAC) on AA toxicity. Materials and methods: Four groups were formed with 9 pregnant rats each as control (C), acrylamide (AA), N-acetylcysteine (NAC), acrylamide plus N-acetylcysteine (AA plus NAC) groups. Caesarian section was implemented on the 20th day of pregnancy. Malondialdehyde (MDA), reduced glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT) and Brain-derived neurotrophic factor (BDNF) levels were analyzed and histopathologic examinations were performed in brain tissues of the fetuses. Results: Our data indicated that AA caused necrotic death and hemorrhagic damages in fetal brain tissue with decreasing BNDF levels and increasing oxidative stress. N-acetylcysteine prevented the toxic effects of its on fetal brain (p < 0.05). Conclusion: Our study indicated that acrylamide has toxic effects in the fetal brain and N-acetylcysteine prevents its toxic effect.
dc.description.sponsorshipScientific Research Fund of Inonu University [INU-BAP-2011/58]
dc.description.sponsorshipThis study was sponsored by a Grant from Scientific Research Fund of Inonu University (Grant number: INU-BAP-2011/58 to Turkoz Y). The authors thank to Mehmet Gul for histopathological preparations.
dc.identifier.doi10.1016/j.ntt.2018.03.005
dc.identifier.endpage43
dc.identifier.issn0892-0362
dc.identifier.issn1872-9738
dc.identifier.pmid29580927
dc.identifier.scopus2-s2.0-85053547437
dc.identifier.scopusqualityQ2
dc.identifier.startpage37
dc.identifier.urihttps://doi.org/10.1016/j.ntt.2018.03.005
dc.identifier.urihttps://hdl.handle.net/11480/15956
dc.identifier.volume67
dc.identifier.wosWOS:000436651500006
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherPergamon-Elsevier Science Ltd
dc.relation.ispartofNeurotoxicology and Teratology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241106
dc.subjectAcrylamide
dc.subjectOxidative stress
dc.subjectN-acetylcysteine
dc.subjectFetal brain development
dc.subjectBrain-derived neurotrophic factor
dc.titleAcrylamide applied during pregnancy causes the neurotoxic effect by lowering BDNF levels in the fetal brain
dc.typeArticle

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