Ureagenesis of Asian seabass (Lates calcarifer) under ammonia stress and overcrowding

Abstract

Ammonia, an excretory substance resulting from the catabolism of proteins and amino acids, is toxic to fish. Increasing ammonia, due to overcrowding fish in a tank, results in dropping production efficiency. This study aims to investigate the adaptation of Asian sea bass to increased ammonia content in fish tanks with different populations. Five groups were tested in 250-l plastic tanks: group A: 15 fish (6 g/L), group B: 20 fish (8 g/L), group C: 25 fish (10 g/L), group D: 30 fish (12 g/L), group E: 35 fish (14 g/L). The ammonia level in the tanks was measured daily. After 60 days, the activity of some enzymes and biochemical parameters related to ammonia was measured in muscle, liver, and blood. The results were statistically analyzed. After hypoxia, in the overcrowded group, the level of liver glycogen and blood glucose fell; the blood lactate and muscle adenosine monophosphate deaminase (AMPD) activity increased; the activity of muscle glutamate dehydrogenase (GDH) increased; the activity of glutamate dehydrogenase, glutaminase, arginase, and aspartate transferase (AST) of the liver increased. Due to the increased activity of urea cycle enzymes in the liver, urea was detected in the blood. One of the strategies that Asian sea bass adopts in dealing with a high level of ammonia is to activate the urea cycle in the liver and turn ammonia into urea to control it. This way is a type of adaptation to ammonia stress that was not identified in this species before.