Effects of ammonia-N exposure on the growth, metabolizing enzymes, and metabolome of Macrobrachium rosenbergii

摘要

Ammonia nitrogen elevated is one of the commonest problem in the aquatic system, which caused a great threat to the survival and growth of prawn. However, little is know about the ammonia metabolism and detoxification strategy of prawn. In this study, the effects of ammonia-N (0, 0.108, 0.216, 0.324, or 0.54 mg L-1) on growth and metabolizing enzymes in hepatopancreas of Macrobrachium rosenbergii, including glutamine synthetase (GS), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and glutamate dehydrogenase (GDH), were investigated. The metabolome of its muscle was also analyzed after exposure to ammonia-N (0, 0.108, 0.324, or 0.54 mg L-1) for 20 days. The survival rate of M. rosenbergii decreased significantly after treatment with 0.54 mg L-1 ammonia-N compared with that in the other groups. However, ammonia-N had no significant effect on the growth of the river prawn after exposure for 20 days. GS activity increased significantly after exposure to 0.108 mg L-1 ammonia-N compared with the control and other ammonia-N-treated groups. Hepatopancreatic GDH activity was lower in the prawns treated with 0.216, 0.324, or 0.54 mg L-1 ammonia-N than in the control by 34.70%, 38.80%, or 41.94%, respectively. Ammonia-N had no significant effect on hepatopancreatic AST or ALT activity. Urea nitrogen was higher in the prawns treated with 0.216 mg L-1 ammonia-N than in the control or those treated with 0.54 mg L-1 ammonia-N. Ammonia-N had significant effects on the lipid, carbohydrate. and protein metabolism of M. rosenbergii, including purine metabolism, amino sugar and nucleotide sugar metabolism, a-linolenic acid metabolism, arginine and proline metabolism, glutathione metabolism, and phosphonate and phosphate metabolism, and on the terpenoid biosynthesis, lysine degradation, and lysine biosynthesis pathways. High concentrations of ammonia-N stress increased the content of glutamate and arginine, which may participate in the urea cycle, which synthesizes glutamine or urea to eliminate ammonia toxicity.