Waterborne copper exposure decreases fish growth and survival by promoting gills and liver impairments in largemouth bass (Micropterus salmoides).

The study aimed to investigate the effect of Cu exposure (0, 51.3, 164, 513, 1,640, and 5,130 μg/L) on fish growth performance, histology, oxidative stress, inflammation, and apoptosis in largemouth bass (Micropterus salmoides) juveniles. 270 fish (2.69 ± 0.02 g) were randomly divided into 6 groups of tanks for 4 weeks with each group comprising three replicate tanks. The results showed that fish exposed to 1,640 and 5,130 μg/L Cu exhibited a significant reduction in fish growth and survival rate (P < 0.05). Compared to the control, the fish at and above 513 μg/L Cu demonstrated histopathological damages in the gills and liver, such as shorter primary and secondary lamellae, smaller hepatocyte nuclei, and an increase in the number of necrotic cells in the liver. Compared to the control, fish at and above 1,640 μg/L Cu had a significantly higher malondialdehyde content and lower activity levels of total superoxide dismutase, glutathione peroxidase, and catalase in the gills and liver (P < 0.05). Furthermore, high concentrations of Cu (1,640 and 5,130 μg/L) significantly increased hepatic inflammation by upregulating interleukin-1β and tumor necrosis factor α expression and hepatic apoptosis by increasing cysteinyl aspartate specific protease 3 (caspase-3) and caspase-9 expression (P < 0.05). Pearson correlation analysis showed that fish growth and survival positively correlated with histological and antioxidant defense parameters, and negatively correlated with oxidative stress parameters, hepatic inflammation, and hepatic apoptosis. Taken together, these results suggest that high levels of waterborne Cu can induce growth retardation and mortality by damaging the liver and gill health.