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    Acrylamide applied during pregnancy causes the neurotoxic effect by lowering BDNF levels in the fetal brain
    (Pergamon-Elsevier Science Ltd, 2018) Erdemli, Mehmet Erman; Aladag, M. Arif; Altinoz, Eyup; Demirtas, Sezin; Turkoz, Yusuf; Yigitcan, Birgul; Bag, Harika Gozukara
    Objectives: 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.
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    Acrylamide applied during pregnancy causes the neurotoxic effect by lowering bdnf levels in thefetal brain
    (Pergamon-elsevıer scıence ltd, the boulevard, langford lane, kıdlıngton, oxford ox5 1gb, england, 2018) Erdemli, Mehmet Erman; Aladag, M. Arif; Altinoz, Eyup; Demirtas, Sezin; Turkoz, Yusuf; Yigitcan, Birgul; Bag, Harika Gozukara
    Objectives: 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.
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    Hesperidin attenuates oxidative and neuronal damage caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model
    (Springer-Verlag Italia Srl, 2014) Oztanir, M. Namik; Ciftci, Osman; Cetin, Asli; Aladag, M. Arif
    The aim of this study was to determine the effects of hesperidin (HP) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. For this purpose, a total of 40 mice were divided equally into four groups: (1) sham-operated (SH), (2) global cerebral I/R, (3) HP, and (4) HP+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with vehicle for 10 days. In the HP group, mice were administered HP (100 mg/kg) for 10 days without carotid occlusion. In the HP+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with 100 mg/kg HP for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidation and a decrease in the components of the antioxidant defense system. Furthermore, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue. HP treatment significantly reversed the oxidative effects of I/R and inhibited the development of neurodegenerative histopathology. Therefore, the current study demonstrates that HP treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, the beneficial effects of HP are likely a result of its strong antioxidant and free radical-scavenging properties. HP may be an useful treatment to attenuate the negative effects of global cerebral I/R.