Abstract
The point of our study was to examine the interaction of ammonia-N poisoning and salinity on serum enzymes and oxidative stress factors of blood and liver in Nile tilapia (Oreochromis niloticus). The 50% lethal concentration (LC(50)) in 96 h was 0.86 mg/L of ammonia-N. A random allocation was used to divide the fish into 12 treatments. These treatments encompassed various combinations of acute ammonia-N levels (0 and 50% of LC(50)-96 h), sub-acute ammonia-N levels (30% of LC(50)-96 h), and salinity levels (0, 4, 8, and 12 ppt). The experimental design employed a factorial arrangement of 3 × 4.The findings revealed that the amounts of aspartate transferase (AST) and alanine transaminase (ALT) in treatments 3 and 4 increased significantly compared to the treatment 2 (4 ppt) and control. Salinity levels did not affect serum glutathione levels (GSH), nevertheless the reduction of serum GSH and levels of total antioxidant capacity (TAC) and superoxide dismutase (SOD) and catalase activities (CAT) in ammonia poisoning treatments, 5 and 9, compared to the control, states ammonia can stimulate oxidative stress in fish. Similar to the serum measurements, increasing salinity in acute ammonia poisoning treatments (5, 6, 7 and 8) caused an increasing effect on the liver TAC value, which was presumably due to the improving effect of salinity in reducing ambient ammonia. The findings indicate that while elevated salinity levels can be beneficial in mitigating the effects of ammonia toxicity in water, the combined presence of salinity, ammonia, and their interaction had detrimental impacts on the physiological well-being of fish over a 96-hour testing period.