Establishment of hyperammonemia mode in yellow catfish and the mitigation of exogenous L-ornithine-L-aspartate

Abstract

Ammonia stress can lead to fish ammonia poisoning. The l-ornithine-l-aspartate (LoLa) has potential value in treating fish hyperammonemia. This study tried to establish a hyperammonemia mode of yellow catfish, which was used to evaluate the effect of LoLa on hyperammonemia. Fish were injected with ammonium acetate and sodium chloride for 3 d to establish model, respectively. Then ammonium acetate group was divided into two groups: one group was further injected with ammonium acetate, another group was injected with LoLa. Sodium chloride group was also divided into two groups: one group was further injected with sodium chloride, another group was injected with LoLa. The experiment continued for 96 h. The results showed that ammonia poisoning could induce serum ammonia content elevated, liver damage (serum aminotransferase activity elevated and liver malondialdehyde accumulation), and up-regulation of cytokine (IL 1, IL 8 and TNFɑ), apoptosis (P53, Bax, Cytochrome c, Caspase 3 and Caspase 9) and autophagy (Dynein, Beclin 1, AKT and PTEN) genes transcription, but LoLa could mitigate the adverse effect of ammonia poisoning. Our results suggesting that LoLa can detoxify ammonia into glutamine and stores it in muscle.

Keywords: Ammonia; Glutamine; Hyperammonemia mode; Pelteobagrus fulvidraco; l-ornithine-l-aspartate.