Awad Mohamed A, Ahmed Zainab Sabry Othman, AbuBakr Huda O, Elbargeesy Gehad Abd El-Fattah Hassan, Moussa Moukhtar H G
Department of Cytology and Histology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
Department of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt.
Environ Sci Pollut Res Int. 2022 Jan;29(1):936-948. doi: 10.1007/s11356-021-15537-3. Epub 2021 Aug 3.
Fipronil (FIP) is a highly effective insecticide that has been used in agriculture and veterinary medicine. Its neurotoxic effect to insects and to non-target organisms, after nonintentional exposure, was reported. Many studies were conducted to evaluate FIP effects on mammals. However, slight is known about its effect on the brain stem and diencephalon. The current study was designed to investigate the ability of FIP to induce oxidative stress as a molecular mechanism of FIP neurotoxicity that resulted in apoptosis and neural tissue reactivity in these regions. Ten adult male rats received 10 mg/kg of FIP technical grade by oral gavage, daily for 45 days. Brain stem and diencephalon were processed to examine oxidative stress-induced macromolecular alteration (MDA, PCC and DNA fragmentation). Also, the histopathological assessment and immunoreactivity for caspase-3 (active form), iNOS and GFAP were performed on the thalamus, hypothalamus and medulla oblongata. Our results revealed that FIP significantly raised MDA, PCC and DNA fragmentation (p ≤ 0.05). In addition, significantly increased immunoreactivity to GFAP, iNOS and caspase-3 (active form) in the FIP-treated group was noticed (p ≤ 0.05). Moreover, alterations in the histoarchitecture of the neural tissue of these regions were observed. We conclude that FIP can induce oxidative stress, leading to apoptosis and tissue reaction in brain stem and diencephalon.
氟虫腈（FIP）是一种高效杀虫剂，已用于农业和兽医学领域。据报道，非故意接触后，它对昆虫和非靶标生物具有神经毒性作用。人们进行了许多研究来评估氟虫腈对哺乳动物的影响。然而，关于其对脑干和间脑的影响却知之甚少。本研究旨在探究氟虫腈诱导氧化应激的能力，这是氟虫腈神经毒性的一种分子机制，可导致这些区域的细胞凋亡和神经组织反应性。十只成年雄性大鼠每天经口灌胃给予10mg/kg的氟虫腈原药，持续45天。对脑干和间脑进行处理，以检测氧化应激诱导的大分子改变（丙二醛、蛋白质羰基化和DNA片段化）。此外，还对丘脑、下丘脑和延髓进行了组织病理学评估以及半胱天冬酶-3（活性形式）、诱导型一氧化氮合酶和胶质纤维酸性蛋白的免疫反应性检测。我们的结果显示，氟虫腈显著提高了丙二醛、蛋白质羰基化和DNA片段化水平（p≤0.05）。此外，在氟虫腈处理组中，观察到胶质纤维酸性蛋白、诱导型一氧化氮合酶和半胱天冬酶-3（活性形式）的免疫反应性显著增加（p≤0.05）。此外，还观察到这些区域神经组织的组织结构发生了改变。我们得出结论，氟虫腈可诱导氧化应激，导致脑干和间脑的细胞凋亡和组织反应。
