Oxidative stress and inflammatory responses in the liver of swamp eel (Monopterus albus) exposed to carbon tetrachloride

“Liver and gall syndrome” disease often caused dramatic economic losses in swamp eel (Monopterus albus) which is one of the most economically important freshwater aquaculture fish in China. Carbon tetrachloride (CCl4)-induced liver injury model has been evidenced as a useful method to screen the hepatoprotective agents to study and prevent this disease in fish. Therefore, in order to provide a better research platform for prevention and treatment liver diseases in swamp eel, we evaluated the hepatotoxicity effects of CCl4 on swamp eel based on the acute toxicity and biochemical responses of glutamate pyruvate transaminase (GPT), glutamate oxalate transaminase (GOT), lactate dehydrogenase (LDH), catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA), as well as mRNA expression levels of cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LO). The 96 h LD50 value of CCl4 in swamp eel was 2.54 g/kg. Sublethal levels of CCl4 induced time-depended liver injury in swamp eel, evidenced by the significant increases of serum GPT, GOT and LDH levels at the first 48 h injection, but restoration after 96 h injection. CCl4 led to oxidative stress, supported by the enhanced of MDA contents, and decreased of SOD and CAT activities. Moreover, CCl4 caused hepatic inflammatory reaction, evidenced by the significant changes of the transcription of COX and 5-LO genes in liver tissues. Overall, our results suggested that lipid peroxidation, antioxidant enzymes and COX and 5-LO pathways are important mechanisms involved in CCl4-induced liver injury, and could be used as the effective biomarkers of CCl4-induced liver injury model to screen the hepatoprotective agents in swamp eel.