Department of Medical Biochemistry, Medical Faculty, Ömer Halisdemir University, Niğde, Turkey.
Department of Neurosurgery, Faculty of Medicine, İnönü University, Malatya, Turkey.
Neurotoxicol Teratol. 2018 May-Jun;67:37-43. doi: 10.1016/j.ntt.2018.03.005. Epub 2018 Mar 24.
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.
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.
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).
Our study indicated that acrylamide has toxic effects in the fetal brain and N-acetylcysteine prevents its toxic effect.
本研究旨在阐明丙烯酰胺（AA）在妊娠期间对胎儿大脑发育的神经毒性作用的可能机制，并展示 N-乙酰半胱氨酸（NAC）对 AA 毒性的影响。
将 9 只孕鼠分为 4 组，分别为对照组（C）、丙烯酰胺组（AA）、N-乙酰半胱氨酸组（NAC）、丙烯酰胺加 N-乙酰半胱氨酸组（AA 加 NAC）。在妊娠第 20 天进行剖腹产。分析胎鼠脑组织中丙二醛（MDA）、还原型谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和脑源性神经营养因子（BDNF）水平，并进行组织病理学检查。
我们的数据表明，AA 导致胎儿脑组织发生坏死性死亡和出血性损伤，同时降低 BDNF 水平，增加氧化应激。N-乙酰半胱氨酸可预防其对胎儿大脑的毒性作用（p<0.05）。
本研究表明丙烯酰胺对胎儿大脑具有毒性作用，而 N-乙酰半胱氨酸可预防其毒性作用。
