Ammonia Toxicity in the Bighead Carp (Aristichthys nobilis): Hematology, Antioxidation, Immunity, Inflammation and Stress

Ammonia is one of the main environmental pollutants that affect the survival and growth of fish. The toxic effects on blood biochemistry, oxidative stress, immunity, and stress response of bighead carp (Aristichthys nobilis) under ammonia exposure were studied. Bighead carp were exposed to total ammonia nitrogen (TAN) concentrations of 0 mg/L, 3.955 mg/L, 7.91 mg/L, 11.865 mg/L, and 15.82 mg/L for 96 h. The results showed that ammonia exposure significantly reduced hemoglobin, hematocrit, red blood cell, white blood cell count, and platelet count and significantly increased the plasma calcium level of carp. Serum total protein, albumin, glucose, aspartate aminotransferase, and alanine aminotransferase changed significantly after ammonia exposure. Ammonia exposure can induce intracellular reactive oxygen species (ROS), and the gene expression of antioxidant enzymes (Mn-SOD, CAT, and GPx) increases at the initial stage of ammonia exposure, while MDA accumulates and antioxidant enzyme activity decreases after ammonia stress. Ammonia poisoning changes the gene expression of inflammatory cytokines; promotes the gene expression of inflammatory cytokines TNF-alpha, IL-6, IL-12, and IL-1 beta; and inhibits IL-10. Furthermore, ammonia exposure led to increases in stress indexes such as cortisol, blood glucose, adrenaline, and T3, and increases in heat shock protein 70 and heat shock protein 90 content and gene expression. Ammonia exposure caused oxidative stress, immunosuppression, inflammation, and a stress reaction in bighead carp.

Automated summary

The toxic effects of ammonia exposure on blood biochemistry, oxidative stress, immunity, and stress response in bighead carp were studied. The results showed that ammonia exposure significantly affected the blood parameters of carp and induced oxidative stress, immunosuppression, inflammation, and stress.