Growth performance, physiological response and histology changes of juvenile blunt snout bream, Megalobrama amblycephala exposed to chronic ammonia

Abstract

Ammonia is one of the major environmental pollutants in freshwater aquatic systems that affects the survival and growth of organisms. In the present study, a nine-week experiment was conducted to investigate the chronic toxicity of ammonia on survival and selected hematological parameters, antioxidant ability, and histological structure in juvenile Chinese blunt snout bream, Megalobrama amblycephala. Fish were exposed to one of five different ammonia concentrations (0, 5, 10, 15, and 20 mg L −1 total ammonia-N, pH = 7.86 ± 0.41, temperature = 28.23 ± 0.79 °C). Growth performance of fish in the high-ammonia treatment was lower than that of fish in the control group. The survival rate in the group exposed to the highest ammonia-N concentration (20 mg L−1) was significantly lower than that of the control group. The lowest level of white blood cell count (WBC), red blood cell count (RBC), hemoglobin, hematocrit, and plasma glucose and the highest level of plasma ammonia, cortisol and aspartate transaminase were observed in fish exposed to ammonia-N at 20 mg L −1 compared with the control group. The liver superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities in fish exposure to 20 mg L −1 ammonia-N group were significantly lower than those in the control group, while oxidative stress indices (levels of malondialdehyde, MDA) was significantly higher than those in the control group. Regression analysis found that growth performance, plasma parameters, hematological parameters, and antioxidant status of fish were significant linear correlated to ammonia-N concentration. Fish exposed to various concentrations of ammonia displayed histopathologic alterations in both gill and liver tissue. Furthermore, morphological examination by transmission electron microscopy revealed that gill tissues displayed vacuolation of the cytoplasm, damaged mitochondria, increased heterochromatin, and intense desquamation of pavement epithelial cells on the gill lamellae. Our findings suggest that the stress responses induced in juvenile blunt snout bream by chronic exposure to ammonia are not limited to simple growth inhibition, but are accompanied by changes in oxidative stress, plasma parameter effects, and alterations in the histology of the liver and gill. Blunt snout bream had a dose-dependent effect on ammonia-N. We preliminarily suggest that the level of plasma ammonia, MDA, CAT, AST, FER, and SGR can be used as an indicator for chronic ammonia-N toxicity, but further research and verification are needed in the future.