We investigated the ammonia metabolism pathway of after acute carbonate alkalinity gradient stresses, and studied several ammonia metabolism-related genes:glutamine synthetase (), carbamyl phosphate synthetase 1(); serum ammonia concentration; gene expression; and enzyme activity. The serum ammonia concentration increased as the carbonate alkalinity gradient rose, and showed a trend to increase and then decrease, with the greatest at 12 h. Ammonia metabolism-related genes in different tissues were up regulated to various degrees after different alkalinity stresses. The expression change trends showed an increase and then a decrease over time; their expression increased significantly at 12-24 h, then recovered gradually to stable levels. were mainly expressed in the liver; and was mainly expressed in the kidney and gill. Enzyme activity results showed that CA and GS activities increased along with increased alkalinity, and that CA acted most significantly in the gill and GS in the liver. Overall, the results showed that carbonate alkalinity stress can result in the raising of serum ammonia concentrations, and that ammonia metabolism-related genes in the gill, liver and kidney played different roles in adjusting to ammonia metabolism:excreting the ammonia directly in the gill, producing glutamine and urea in the liver, and decreasing the serum ammonia concentration.