The first report of AMP-deaminase activity in skeletal muscles of Lates calcarifer and its stunning adaptation to ammonia poisoning.

Ammonia poisoning is a common issue in fish breeding systems, leading to complications such as hypoxia and cellular energy crises. The AMP-deaminase enzyme plays a crucial role in maintaining the ATP/AMP ratio and responding to energy deficits. This study investigates the adaptation of AMP-deaminase in Asian sea bass (Lates calcarifer) to ammonia stress. A total of 150 fish were divided into two groups with densities of 6 g/L (control) and 14 g/L (densely stock fish), each replicated three times over 60 days. Ammonia levels increased significantly in both groups (P < 0.0001), with a higher concentration in the densely stock fish (> 1.6-fold increase compared to control, P < 0.001). The enzyme activity showed a significant enhancement in the densely stock fish, with Kcat increasing from 1.85 to 2.70 S^-1 and Vmax decreasing from 11.99 to 8.10 μmol/mg s. The enzyme's stability was significantly higher in adverse conditions, as evidenced by an extended half-life (7 vs. 6 days in control, P < 0.05) and increased resistance to urea denaturation (I50 at 1.6 mM vs. 0.8 mM in control, P < 0.01). Optimal pH shifted from 7 (control) to 6 (densely stocked fish, P < 0.05), indicating an adaptation to acidic conditions. Additionally, enzyme activity remained stable under oxidative stress (H₂O₂ + FeSO₄ exposure) and exhibited a significantly lower activation energy in the densely stock fish (14.1 vs. 17.98 kJ/mol, P < 0.05). These findings indicate that the AMP-deaminase enzyme in Lates calcarifer adapts to ammonia-induced hypoxia by modifying its kinetic properties and structural stability, enhancing muscle resilience under environmental stress. Further genetic and metabolic studies will strengthen these findings.