College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China.
College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, China; Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, Harbin, 150030, China.
Environ Pollut. 2021 Oct 1;286:117319. doi: 10.1016/j.envpol.2021.117319. Epub 2021 May 6.
Deltamethrin is the most common type II synthetic pyrethroid insecticide, and has posed widespread residues to environment. However, whether deltamethrin has potential toxic effects on quail cerebrum remains greatly obscure. Accordingly, we investigated the impact of chronic exposure to deltamethrin on oxidative stress and apoptosis in quail cerebrum. Quails upon 12-week exposure of deltamethrin (0, 15, 30, or 45 mg/kg body weight intragastric administration) were used as a cerebrum injury model. The results showed that deltamethrin treatment led to cerebral injury dose-dependently through the weakened antioxidant defense by downregulating nuclear factor erythroid-2-related factor 2 (Nrf2) and its downstream proteins levels and mRNA expression. Furthermore, deltamethrin treatment induced apoptosis in cerebrum by decreasing B-cell lymphoma gene 2 (Bcl-2) level, as well as increasing Jun N-terminal kinase3, caspase-3, and Bcl-2-associated X protein levels. Simultaneously, toll-like receptor 4 (TLR4) downstream inflammation-related genes or proteins were significantly up-regulated by deltamethrin dose-dependently. Altogether, our study demonstrated that chronic exposure to deltamethrin induces inflammation and apoptosis in quail cerebrums by promoting oxidative stress linked to inhibition of the Nrf2/TLR4 signaling pathway. These results provide a novel knowledge on the chronic toxic effect of deltamethrin, and establish a theoretical foundation for the evaluation of pesticide-induced health risk.
溴氰菊酯是最常见的 II 型合成拟除虫菊酯杀虫剂，对环境造成了广泛的残留。然而，溴氰菊酯是否对鹌鹑大脑有潜在的毒性作用仍不清楚。因此，我们研究了慢性暴露于溴氰菊酯对鹌鹑大脑氧化应激和细胞凋亡的影响。鹌鹑经过 12 周的溴氰菊酯（0、15、30 或 45mg/kg 体重灌胃）暴露，作为大脑损伤模型。结果表明，溴氰菊酯处理通过下调核因子红细胞 2 相关因子 2（Nrf2）及其下游蛋白水平和 mRNA 表达，减弱抗氧化防御，导致大脑损伤呈剂量依赖性。此外，溴氰菊酯处理通过降低 B 细胞淋巴瘤基因 2（Bcl-2）水平，增加 Jun N-末端激酶 3、caspase-3 和 Bcl-2 相关 X 蛋白水平，诱导大脑细胞凋亡。同时，溴氰菊酯呈剂量依赖性地显著上调 Toll 样受体 4（TLR4）下游炎症相关基因或蛋白。总之，我们的研究表明，慢性暴露于溴氰菊酯通过促进与 Nrf2/TLR4 信号通路抑制相关的氧化应激，引起鹌鹑大脑的炎症和细胞凋亡。这些结果为溴氰菊酯的慢性毒性作用提供了新的认识，并为评估农药引起的健康风险奠定了理论基础。
