Abstract
The red swamp crayfish (Procambarus clarkii), widely farmed in China, frequently suffers from hepatopancreatic diseases due to the expansion and environmental degradation of aquaculture. Hepatopancreatic injury models are essential for studying disease mechanisms and treatments, yet few exist for crustaceans. This study aims to establish a hepatopancreatic injury model in P. clarkii using the hepatotoxic compound thioacetamide (TAA) and investigate the underlying damage mechanisms. P. clarkii were intramuscularly injected with TAA at concentrations of 0.2, 0.4, and 0.8 mg/g and observed at 6, 12, 24, and 48 h. The results showed that TAA at 0.2–0.8 mg/g significantly affected hepatopancreatic function and oxidative stress-related enzymes in P. clarkii. However, only 0.8 mg/g TAA produced a time-dependent damage effect suitable for a hepatopancreatic injury model. Histopathological analysis revealed that P. clarkii injected with 0.8 mg/g TAA exhibited key model features, including R cell adhesion and swelling, hepatic tubule rupture, and numerous small vacuoles. Therefore, 0.8 mg/g TAA intramuscular injection can effectively establish a hepatopancreatic injury model in P. clarkii. Transcriptomic and metabolomic analyses revealed that metabolic disruptions in energy, amino acid, lipid, and nucleotide pathways are central to TAA-induced hepatopancreatic injury in P. clarkii. CYP2L1X1, CYP2U1lX1, and CYP2D14l are likely key contributors to the hepatopancreatic injury induced by TAA in P. clarkii. The results of this study will provide support for further research on the mechanisms of hepatopancreatic diseases in freshwater crayfish and the development of preventive and therapeutic drugs.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call