Erdemli, Mehmet ErmanAladag, M. ArifAltinoz, EyupDemirtas, SezinTurkoz, YusufYigitcan, BirgulBag, Harika Gozukara2024-09-292024-09-2920180892-03621872-9738https://doi.org/10.1016/j.ntt.2018.03.005https://hdl.handle.net/20.500.14619/5174Objectives: 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.eninfo:eu-repo/semantics/closedAccessAcrylamideOxidative stressN-acetylcysteineFetal brain developmentBrain-derived neurotrophic factorArticle10.1016/j.ntt.2018.03.0052-s2.0-850535474374329580927Q23767WOS:000436651500006Q2