Establishment and mechanism of thioacetamide-induced hepatopancreas injury model in red swamp crayfish Procambarus clarkii

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. • A hepatopancreatic injury model for Procambarus clarkii was established. • Characteristic damage features was found post- thioacetamide intramuscular injection . • The optimal induction condition is 0.8 mg/g thioacetamide for 12–24 h. • Thioacetamide causes hepatopancreatic injury by disrupting multiple metabolic pathways. • These findings support further research on hepatopancreatic diseases and drug development.