Acute effects of ammonia on antioxidative response and gill Na+/K+ ATPase activity of juvenile Australian red claw crayfish (Cherax quadricarinatus)

The acute toxicity of ammonia to juvenile Cherax quadricarinatus was evaluated. The 24-, 48-, 72-, and 96-h LC50 values of total ammonia nitrogen (TAN) were 51.02 (44.58-58.43), 24.99 (19.17-32.89), 17.83 (13.50-37.22), and 15.38 (8.50-27.94) mg L-1 while the LC50s of unionized ammonia nitrogen (NH3-N) were 1.19 (1.04-1.37), 0.58 (0.45-0.77), 0.42 (0.32-0.87), and 0.36 (0.20-0.65) mgL(-1), respectively. The safe concentration of ammonia (NH3) for juvenile C. quadricarinatus was TAN 1.8 mg L-1 (NH3-N = 0.04mg L-1, pH 7.6, 26 degrees C). LC50 of NH3 decreased significantly with time and fitted a hyperbolic decay model well. Based on the LC50 values, a 96-h NH3 exposure was then conducted, using four test concentrations (4, 8, 12, and 16 mg L-1 TAN) plus a control group. Hepatopancreas catalase (CAT) and superoxide dismutase (SOD) activities fluctuated with time and NH3 concentration and had a similar trend at 24 and 48 h. Both exhibited a peak after 24 h of exposure to 8mg L-1 TAN and did not change significantly at 48 h. At 96 h, SOD activity significantly decreased with increasing NH3 concentration while CAT activity remained unchanged. Malondialdehyde (MDA) level in hepatopancreas did not change in any groups at 24 h. At 48 and 96 h, it increased as NH3 concentration increased. There was no significant interaction between time and NH3 concentration on SOD, CAT, nor MDA. After 96 h, notable depressions of the gill Na+/K+ ATPase activity were observed in high NH3 concentration groups. The results suggest that the observed lethal toxicity of NH3 could be related to a gradual dysfunction of antioxidant systems and Na+/K+ ATPase activity leading to antioxidant system and osmoregulatory depression. The results will be helpful to aquaculture farmers in preventing depression of productivity caused by elevated NH3.