Department of Pathology, Faculty of Veterinary Medicine, Cairo University, P.O. Box 12211, Giza, Egypt.
Department of Toxicology and Forensic Medicine, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt.
Environ Sci Pollut Res Int. 2022 Apr;29(19):29091-29104. doi: 10.1007/s11356-021-18486-z. Epub 2022 Jan 7.
Pesticides are viewed as a major wellspring of ecological contamination and causing serious risky consequences for people and animals. Imidacloprid (IM) and hexaflumuron (HFM) are extensively utilized insect poisons for crop assurance on the planet. A few investigations examined IM harmfulness in rodents, but its exact mechanism hasn't been mentioned previously as well as the toxicity of HFM doesn't elucidate yet. For this reason, the present study was designed to explore the mechanism of each IM and HFM-evoked rat liver and kidney toxicity and to understand its molecular mechanism. 21 male Wistar albino rats were divided into 3 groups, as follows: group (1), normal saline; group (2), IM; and group (3), HFM. Both insecticides were orally administered every day for 28 days at a dose equal to 1/10 LD50 from the active ingredient. After 28 days postdosing, rats were anesthetized to collect blood samples then euthanized to collect liver and kidney tissue specimens. The results showed marked changes in walking, body tension, alertness, and head movement with a significant reduction in rats' body weight in both IM and HFM receiving groups. Significant increases in MDA levels and decrease of GHS levels were recorded in liver and kidney homogenates of either IM or HFM groups. Liver and kidney tissues obtained from both pesticide receiving groups showed extensive histopathological alterations with a significant increase in the serum levels of ALT, AST, urea, and creatinine and a decrease in total proteins, albumin, and globulin levels. In addition, there was upregulation of the transcript levels of casp-3, JNK, and HO-1 genes with strong immunopositivity of casp-3, TNF-ὰ, and NF-B protein expressions in the liver and kidneys of rats receiving either IM or HFM compared with the control group. In all studied parameters, HFM caused hepatorenal toxicity more than those induced by IM. We can conclude that each IM and HFM provoked liver and kidneys damage through overproduction of ROS, activation of NF-B signaling pathways and mitochondrial/JNK-dependent apoptosis pathway.
农药被视为生态污染的主要源头,对人类和动物造成严重的风险后果。吡虫啉(IM)和六氟灵(HFM)是世界范围内广泛用于作物保护的杀虫剂。一些研究调查了 IM 对啮齿动物的危害性,但之前没有提到其确切的机制,也没有阐明 HFM 的毒性。因此,本研究旨在探讨 IM 和 HFM 诱发大鼠肝肾功能毒性的机制,并了解其分子机制。将 21 只雄性 Wistar 白化大鼠分为 3 组,如下:组(1),生理盐水;组(2),IM;组(3),HFM。两种杀虫剂均以相当于活性成分 LD50 的 1/10 剂量每天口服给药,共 28 天。给药 28 天后,麻醉大鼠收集血液样本,然后处死收集肝、肾组织标本。结果显示,IM 和 HFM 组大鼠行走、身体张力、警觉性和头部运动均出现明显变化,体重明显减轻。在 IM 或 HFM 组的肝、肾匀浆中均记录到 MDA 水平显著升高,GSH 水平显著降低。从两种农药处理组获得的肝、肾组织均表现出广泛的组织病理学改变,血清 ALT、AST、尿素和肌酐水平显著升高,总蛋白、白蛋白和球蛋白水平降低。此外,与对照组相比,IM 或 HFM 处理组大鼠肝、肾组织中 caspase-3、JNK 和 HO-1 基因的转录水平上调,caspase-3、TNF-ὰ 和 NF-B 蛋白表达的免疫阳性增强。在所有研究参数中,HFM 引起的肝肾功能毒性大于 IM 引起的毒性。我们可以得出结论,IM 和 HFM 均通过 ROS 的过度产生、NF-B 信号通路和线粒体/JNK 依赖性细胞凋亡通路的激活引起肝、肾损伤。