College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Comp Biochem Physiol C Toxicol Pharmacol. 2021 Nov;249:109126. doi: 10.1016/j.cbpc.2021.109126. Epub 2021 Jul 1.
Chlorpyrifos (CPF) is an organophosphate insecticide and can cause cell death of animals. In the study, the common carp were exposed to CPF at 0 μg/L (the control group), 1.16 μg/L (the low dose group), 11.6 μg/L (the medium dose group), and 116 μg/L (the high dose group), respectively. The carp were euthanized at the 30th day and gills were collected immediately. The ultrastructural and histopathological observations showed obvious necrosis characteristics and inflammatory injury in the CPF-treated groups. CPF exposure activated the MAPK pathway, in which the mRNA and protein expressions of extracellular signal-regulated (ERK), p38 MAP kinase (p38), and c-Jun N-terminal kinase (JNK) were increased; the mRNAs and proteins of NF-κB and TNF-α were activated; and the mRNAs and proteins of necroptosis related genes were changed (the mRNA and protein expression of RIPK1, RIPK3, MLKL, and FADD were increased and caspase-8 was decreased) with concentration dependency. Taken together, we concluded that CPF exposure activated the MAPK/NF-κB/TNF-α pathway, promoted inflammatory injure and evoked necroptosis in common carp gills. In addition, CPF-induced inflammation and necroptosis was concentration dependency. The toxic effects of CPF on gills provided data for both aquaculture and toxicological studies.
毒死蜱（CPF）是一种有机磷杀虫剂，可导致动物细胞死亡。在这项研究中，鲫鱼分别暴露于 0μg/L（对照组）、1.16μg/L（低剂量组）、11.6μg/L（中剂量组）和 116μg/L（高剂量组）的 CPF 中。第 30 天处死鲫鱼并立即采集鳃。超微结构和组织病理学观察显示，CPF 处理组出现明显的坏死特征和炎症损伤。CPF 暴露激活了 MAPK 通路，其中细胞外信号调节激酶（ERK）、p38 丝裂原活化蛋白激酶（p38）和 c-Jun N 末端激酶（JNK）的 mRNA 和蛋白表达增加；NF-κB 和 TNF-α 的 mRNAs 和蛋白被激活；并且与坏死相关的基因的 mRNAs 和蛋白发生变化（RIPK1、RIPK3、MLKL 和 FADD 的 mRNA 和蛋白表达增加，caspase-8 减少），具有浓度依赖性。总之，我们得出结论，CPF 暴露激活了 MAPK/NF-κB/TNF-α 通路，促进了鲫鱼鳃的炎症损伤和坏死。此外，CPF 诱导的炎症和坏死具有浓度依赖性。CPF 对鳃的毒性作用为水产养殖和毒理学研究提供了数据。
