Inhibition of argininosuccinate synthase (ASS) affected ammonia excretion in yellow catfish Pelteobagrus fulvidraco during acute ammonia poisoning

Abstract Ammonia is toxic to most fish. Different fish have different treatment methods for ammonia toxicity, mainly including urea cycle and glutamine synthesis pathway, depending on their physiological status. A two-stage study was carried out to test the inhibition of argininosuccinate synthase (ASS) effects on ammonia detoxification in hyperammonemia yellow catfish. At the stage 1, fish were injected lethal half concentration (LC50) of ammonium acetate and sampled at 0, 1, 3, 6, 12 and 24 h post-injection. The result found that plasma ammonia content of fish was injected with ammonium acetate reached its highest level at hour 1, which was used as the optimal sampling time in stage 2. At the stage 2, the four experimental groups were carried out: NaCl group was injected intraperitoneally with 0.9% sodium chloride as control; NH3 group was injected with LC50 ammonium acetate; NH3+BPP group was injected with mixture of ammonium acetate and bradykinin-potentiating peptide (BPP); BPP group was injected with BPP. The results showed that inhibition of ASS can lead to accumulation of ammonia in plasma and kidney, and glutamine in liver and kidney; and decreases ASS, argininosuccinate lyase, arginase activates, and ornithine, glutamate, alanine, proline, tyrosine, methionine contents, and increases ornithine transcarbamylase, glutaminase activates, and citrulline, aspartate, arginine, glutamine, histidine, isoleucine, phenylalanine, lysine contents; and result in upregulation of ASS, ASL, CPS 1, OTC, GS and GLS genes expression. This result indicates that the inhibition of ASS in yellow catfish with ammonia poisoning will lead to the urea cycle disorder; yellow catfish can enhance the detoxification capacity of ammonia by improving glutamine synthesis when the urea cycle is inhibited; argininase played an important role in ammonia detoxification of yellow catfish.