Jianqing Chen,Bing Shao,Jinliang Wang,Zhiqiang Shen,Honggui Liu,Shu Li
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.
Chlorpyrifos (CPF) has caused large-scale pollution worldwide and posed a threat to non-target organisms. Baicalein (BAI) is a flavonoid extract with anti-oxidant and anti-inflammatory activities. The gills are the mucosal immune organ and the first physical barrier of fish. However, it is not clear whether BAI counteracts organophosphorus pesticide CPF exposure-caused gill damage. Therefore, we established the CPF exposure and BAI intervention models by adding 23.2 μg/L CPF in water and/or 0.15 g/kg BAI in feed for 30 days. The results showed that CPF exposure could cause gill histopathology lesions. Moreover, CPF exposure led to endoplasmic reticulum (ER) stress, caused oxidative stress and Nrf2 pathway activation, and triggered NF-κB-mediated inflammation reaction and necroptosis in carp gills. BAI adding effectively relieved the pathological changes, and lighten inflammation and necroptosis involving in the elF2α/ATF4 and ATF6 pathways through binding to GRP78 protein. Moreover, BAI could ease oxidative stress, but did not affect Nrf2 pathway in carp gills under CPF exposure. These results suggested that BAI feeding could alleviate necroptosis and inflammation against chlorpyrifos toxicity through elF2α/ATF4 and ATF6 axis. The results partially explained the poisoning effect of CPF, and showed BAI could be act as an antidote for organophosphorus pesticides.
危险品化学品经营许可证（带存储）