Abstract:Ammonia is a major source of water pollution and a cause of fish diseases. The object of this study was to evaluate the effects of ammonia-N stress on the gill Na+/K+-ATPase, the liver microstructure, and serum physiological-biochemical indices of juvenile Verasper variegatus. Experimental fish had an initial average weight of (70.0±5.5) g. Subjects were first exposed to ammonia-N for 96 hours to obtain the median lethal concentration at 96 h. According to the data, we set up a control group and three ammonia-N treatments of which the concentrations were 35 mg/L (low group), 50 mg/L (middle group), and 65 mg/L (high group). In each group the subjects were treated for a series of periods (0, 6, 12, 24, 48 and 96 h). In the gill microstructure, the ammonia-N stress caused changes such as the increase in chloride cells, the shedding of pavement cells, epithelial tissue hyperplasia, the fracture in blood capillaries, the overflow of red blood cells, shortening and curling of thickened gill dice, and the breakage and congestion of the gill cavity. In liver tissue, we observed dissolution of liver nuclei, vacuoles in cells, liver cell degeneration, liquidized cells, blood sinus expansion, hyperemia, and severe congestion. Under the ammonia-N stress the activities of Na+/K+-ATPase and glutathione peroxidase (GSH-PX) were first decreased and then increased, which was significantly different from the control group (P<0.05). The superoxide dismutase (SOD) activity was raised followed by a decrease, and was higher than the control group (P<0.05). After 96-hour treatment with ammonia nitrogen, the malondialdehyde (MDA) concentration became higher than the control group, and there was a positive correlation between the MDA concentration and ammonia nitrogen concentration (P<0.05). Ammonia nitrogen stress also resulted in an increase-decrease change in activities of serum alanine amino transferase (ALP), aspartate amino transferase (AST) and lysozyme (LSZ) (P<0.05). After 96-hour treatment, activities of liver ALT and AST first increased and then decreased, and was significantly lower than the control group (P<0.05). The liver LSZ activity was significantly lower than the control group after 96-hour treatment (P<0.05). These results suggested that ammonia nitrogen stress could cause a variety of impairments in the fish body, including deterioration of the antioxidant system, nonspecific immune system, physiological metabolism, the gill tissue, the respiratory function and the detoxification function. Also it led to the liver tissue hyperemia and the formation of dot lesions.
