Identification of signal pathways for immunotoxicity in the spleen of common carp exposed to chlorpyrifos.

Chlorpyrifos (CPF) is an environmental pollutant due to its high toxicity to aquatic animals. Because CPF was detected in aquatic environments in many countries, it has been widely concerned by researchers. Although the immunotoxicity of CPF to fish had been reported, the immunotoxicity mechanism is still not clear. Recently, transcriptome analysis has become a major method to study the toxic mechanism of pollutants in environmental toxicology. However, the immunotoxicity identification of CPF on fish had not been reported by transcriptome analysis. In the present study, we examined the effects of CPF on organismal system in the spleen of common carp by transcriptome analysis. We have successfully constructed a database of transcriptome analysis of carp spleens under exposure to CPF and found 773 differentially expressed genes (DEGs) (including 498 up-regulated DEGs and 275 down-regulated DEGs) and 4 branches (containing 33 known KEGG pathways). Some genes associated with the 4 pathways (Complement and coagulation cascades, PPAR signaling pathway, Fat digestion and absorption, and Collecting duct acid secretion) contained in organismal system were validated by quantitative real-time PCR and showed significant improvement compared with the control group. Our results indicated that exposure to CPF caused a change in the signal pathways of organismal system in carp spleens. The present study provides new insights into the immunotoxicity mechanism and risk assessment of CPF, as well as references for comparative medicine.

The co-expression of circRNA and mRNA in the thymuses of chickens exposed to ammonia.

Ammonia (NH3) is one of major air pollutants in intensive poultry houses, affecting chicken health. Circular RNA (circRNA) is a novel type of RNA that can regulate gene expression and be associated with various biological activities. However, the changes of circRNA caused by excess NH3 in chickens have not been investigated. We found differentially expressed genes and morphological changes in the thymuses of chickens exposed to NH3 on day 42. We used a combination of RNA deep sequencing, qRT-PCR, and bioinformatic analysis to explore regulatory mechanism of circRNA and mRNA. Transcriptional profiling results showed that 5 circRNA genes and 100 mRNA genes were significantly dyregulated by high NH3. The results from GO items showed that immune response and the regulation of cytokine production were involved in the mechanisms of chickens exposed to NH3. Co-expression analysis found that circRNA-mRNA network was correlated with oxidative stress and inflammation. NH3 exposure decreased mRNA expression of antioxidant-related genes (GPx and GST4) and increased the mRNA expression of inflammation-related genes (IL-1ß, IL-6, IL-8, and iNOS) in chicken thymuses. Histopathologic analysis demonstrated that NH3 caused inflammatory injury in chicken thymuses. In conclusion, the co-expression of circRNA and mRNA took part in chicken thymus inflammatory injury caused by NH3. Our study further enriches the mechanism of NH3 toxicity on chickens, which may be valuable for human and animal health protection.

Ammonia inhalation-mediated mir-202-5p leads to cardiac autophagy through PTEN/AKT/mTOR pathway.

Ammonia is a known environmental pollutant around the world. It leads to the deterioration of air quality and has adverse effects on human health. Although previous studies have demonstrated that ammonia caused some health problems to chickens, it is still unclear whether ammonia causes cardiac toxicity. The functional autophagy is very important for cardiac homeostasis. Therefore, the role of autophagy was investigated in the mechanism of chicken heart damage induced by environmental contaminant ammonia in our present study. The results from the oxidative stress index (SOD, GPx, H2O2, and MDA), NO content, iNOS activity, and transmission electron microscopy indicated that excess ammonia induced oxidative stress and autophagy in the chicken heart. The expression results from miR-202-5p and PTEN/AKT/mTOR (PTEN, LC3-I, LC3-II, p-AKT, AKT, Beclin1, Dynein, ATG5, p-mTOR and mTOR) signaling pathway-related genes further confirmed that excess ammonia induced cardiac autophagy. In conclusion, these results demonstrated that excess ammonia can cause cardiac damage and mediate mir-202-5p to regulate autophagy through PTEN/AKT/mTOR pathway in the chicken heart injury. Our findings will provide a new insight for better assessing the toxicity mechanism of environmental pollutants ammonia on the heart.