Chronic ammonia toxicity induces glutamine accumulation, oxidative damage and immunosuppression of juvenile yellow catfish Pelteobagrus fulvidraco

A study was carried out to test the responses of juvenile yellow catfish Pelteobagrus fulvidraco to ammonia stress and bacterial challenge. The catfish(1. 94 ± 0. 05)g were randomly allocated to 2 groups(control group and exposure group)in triplicate for 56 days ammonia exposure. No differences were found in fish final weight, weight gain and feed efficiency between ammonia group and control group, but hepatosomatic index of fish in ammonia group was significantly higher than that of fish in control group. Ammonia and glutamine contents in the brain of fish in ammonia group were significantly higher than those of fish in control group, but glutamate content was not significantly different compared with the control. Superoxide dismutase, catalase and glutathione peroxidase activities were significantly lower in ammonia group than in control group, but thiobarbituric acid reactive substance content was significantly higher in ammonia group. Lysozyme activity, phagocytic index and respiratory burst of fish in ammonia group were significantly lower compared with the control group. After 14 days infection of Aeromonas hydrophila, cumulative mortality was not significantly different between ammonia group and control group. This study indicated that the glutamine accumulation in the brain was caused by chronic ammonia exposure; the toxic reactive oxygen species is not fully counteracted by the antioxidant enzymes; the immunosuppression is a process of gradual accumulation of immunosuppressive factors. Our findings support the multifactorial pathogenesis of ammonia toxicity in fish exposed to ammonia.