Nile tilapia (Oreochromis niloticus) show high tolerance to acute ammonia exposure but lose metabolic scope during prolonged exposure at low concentration

Ammonia is a respiratory gas that is produced during the process of protein deamination. In the unionised form (NH₃), it readily crosses biological membranes and is highly toxic to fish. In the present study we examined the effects of unionized ammonia (UIA), on the resting oxygen consumption (MO₂), ventilation frequency (f_V), heart rate (HR) and heart rate variability (HRV) in Nile tilapia (Oreochromis niloticus). Fish were either exposed to progressively increasing UIA concentrations, up to 97 µM over a 5 h period, or to a constant UIA level of 7 µM over a 24 h period. For both treatment groups resting MO₂, HR and f_V were recorded as physiological variables. Relative to the control group, the fish groups exposed to the incremental UIA levels did not exhibit significant changes in their MO₂, HR and f_V at UIA concentrations of 4, 10, 35, or 61 µM compared to control fish. Exposure to 97 µM UIA, however, elicited abrupt and significant downregulations (p < 0.05) in all three responses, as MO₂, HR and fv decreased by 25, 54 and 76 % respectively, compared to control measurements. Heart rate became increasingly irregular with increasing UIA concentrations, and heart rate variability was significantly increased at 61 and 97 µM UIA. Prolonged exposure elicited significant changes at exposure 7 µM UIA. Standard (SMR) and maximum metabolic rate (MMR) were significantly reduced, as was the corresponding f_V and HR. It is evident from this study that Nile tilapia is tolerant to short term exposure to UIA up to 61 µM but experience a significant metabolic change under conditions of prolonged UIA exposures even at low concentrations.