Metabolomics and physiological analyses reveal the gill tissue response mechanism in Micropterus salmoides under exposure to environmental concentrations of ammonia

Intensive aquaculture at high densities readily elevates ammonia concentrations in the water to toxic levels, triggering a series of ecotoxicological effects. To explore the toxic effects of continuous exposure to environmentally relevant concentrations of ammonia on juvenile Micropterus salmoides , this work investigated the changes in gill histological structure, physiological enzyme activities, and metabolomics after 21 days of exposure to various ammonia concentrations (0, 4, 8, and 16 mg/L). The results demonstrated that ammonia exposure induced gill damage, leading to significant inhibition of the SOD, GPX activities, and GSH content while elevating the MDA levels and causing oxidative damage. Furthermore, the levels of Attacin, LYS, IgA, and TCR were significantly increased, suggesting that Micropterus salmoides could avoid pathogenic diseases by enhancing innate immune factors and adaptive immune molecules. The Na + /K + -ATPase activity exhibited an initial increase followed by a decrease, inhibiting ammonia transport. The reduction of Ca 2+ /Mg 2+ -ATPase may result in excessive intracellular accumulation of Ca 2+ , leading to cellular homeostasis disruption. The IBR analysis indicated that the Ca 2+ -Mg 2+ -ATPase, MDA, TCR can serve as biomarkers of ammonia exposure. Additionally, Micropterus salmoides may activate the ornithine-urea cycle to reduce ammonia accumulation and eliminate its toxicity under ammonia stress. In conclusion, from the perspective of gill toxicity effects induced by ammonia exposure alone, ammonia concentrations should be controlled within 4 mg/L and adjusted within 3 days. The results of this study have important guiding significance for the healthy cultivation of Micropterus salmoides .