Histological alterations, oxidative stress, and inflammatory response in the liver of swamp eel (Monopterus albus) acutely exposed to copper.

Copper (Cu) is widely used as an essential trace element in diets as well as a therapeutic chemical. However, excessive Cu has deleterious effects on organisms, including teleosts. Although numerous toxic effects of Cu have been reported, the effects of Cu exposure on the swamp eel (Monopterus albus) as well as the underlying mechanisms have not yet been elucidated. In this study, swamp eels were acutely exposed to 100, 200, and 400 μg/L of Cu for 96 h to evaluate liver histopathology, oxidative stress, and inflammation. Dissolution of hepatocyte membrane, vacuolar degeneration, and inflammatory cell infiltration were detected in the livers of the Cu-treated swamp eels, especially in the 400 μg Cu/L group. Cu-induced hepatic dysfunction was further verified by the elevated activities of glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) and transcript levels of GOT and GPT genes. In addition, Cu exposure decreased the activities of total superoxide dismutase T-SOD and catalase (CAT) and the contents of glutathione (GSH) and total antioxidant capacity (T-AOC) and increased the levels of malondialdehyde (MDA). Cu exposure also significantly decreased the transcript levels of glutathione synthetase (GSS) and increased the transcript levels of SOD1, SOD2, CAT, and heme oxygenase-1 (HO-1) genes. Furthermore, pro-inflammatory genes such as interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), and IL-8 were significantly upregulated. These results indicate that Cu induces oxidative stress and inflammatory response and causes pathological changes in the liver of the swamp eel.