标题：Acute effects of ammonia on antioxidative response and gill Na + /K + ATPase activity of juvenile Australian red claw crayfish ( Cherax quadricarinatus)
摘要：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 un-ionized ammonia nitrogen (NH 3 –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) mg L −1 , respectively. The safe concentration of ammonia (NH 3 ) for juvenile C. quadricarinatus was TAN = 1.8 mg L −1 (NH 3 –N = 0.04 mg L −1 , pH 7.6, 26°C). LC50 of NH 3 decreased significantly with time and fitted a hyperbolic decay model well. Based on the LC50 values, a 96-h NH 3 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 NH 3 concentration and had a similar trend at 24 and 48 h. Both exhibited a peak after 24 h of exposure to 8 mg L −1 TAN and did not change significantly at 48 h. At 96 h, SOD activity significantly decreased with increasing NH 3 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 NH 3 concentration increased. There was no significant interaction between time and NH 3 concentration on SOD, CAT, nor MDA. After 96 h, notable depressions of the gill Na + /K + ATPase activity were observed in high NH 3 concentration groups. The results suggest that the observed lethal toxicity of NH 3 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 NH 3 .
