Transcriptome analysis reveals the mechanisms of hepatic injury caused by long-term environmental exposure to atrazine in juvenile common carp (Cyprinus carpio L.)

Atrazine (ATZ) is the second most commonly used herbicide worldwide, resulting in the pollution of water bodies and affecting the economic benefits of aquaculture. ATZ is known to cause liver damage in the common carp, Cyprinus carpio L., one of the most widely cultivated fish in China, but the underlying mechanisms are poorly understood. In this study, juvenile common carp Cyprinus carpio L. were exposed to three different environmental levels (0.4, 0.8, and 1.2 mu g/L) of ATZ for 12 weeks and changes in the liver transcriptomes between the high-dose group and the control group were analyzed. The data showed that different levels of ATZ exposure caused hepatotoxicity in juvenile carp, shown by biochemical parameters and histopathological changes. Comparative transcriptomics showed that high-dose ATZ exposure led to alterations in the expression of various lipid metabolism-related gene changes, including genes associated with metabolic pathways, fatty acid metabolism, and fatty acid elongation. Furthermore, a connection network analysis of the top 100 differentially expressed genes (DEGs) showed a variety of associations between high-dose ATZ-induced liver damage and the principal DEGs, indicating the complexity of hepatotoxicity induced by ATZ. In conclusion, the molecular mechanisms underlying ATZ-triggered hepatotoxicity in juvenile carp are primarily related to impaired lipid metabolism.

Automated summary

In this study, the effects of high-dose atrazine (ATZ) exposure on the liver transcriptome of juvenile common carp were analyzed. The results showed that ATZ exposure at different concentrations caused liver damage in juvenile carp, as indicated by changes in biochemical parameters and histopathological alterations. Comparative transcriptomics revealed alterations in the expression of lipid metabolism-related genes following high-dose ATZ exposure. Furthermore, a network analysis highlighted the complex relationship between high-dose ATZ-induced liver damage and key differentially expressed genes. These findings suggest that impaired lipid metabolism is the primary molecular mechanism underlying ATZ-triggered hepatotoxicity in juvenile carp.