This study aimed to explore how Wuchang bream (Megalobrama amblycephala) survive and defend against the toxicity of ambient total ammonia nitrogen (0, 5, 10, 20 and 30 mg/L TA-N) during 30-day exposure. As a result, hepatic malondialdehyde and protein carbonylation as well as histopathological alterations increased with increasing TA-N level, which suggested that chronic ammonia exposure caused oxidative stress and damage in the liver of fish. Meanwhile, the activities of hepatic total superoxide dismutase (T-SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glucose 6-phosphate dehydrogenase (G6PD) as well as the mRNA expression of Cu/Zn sod, cat, gpx and g6pd were elevated significantly along with significant reduction of glutathione (GSH) and nicotinamide adenine dinucleotide phosphate (NADPH) (P < 0.05). These results indicated that hepatic antioxidant responses were activated to alleviate oxidative damages induced by ammonia, in which lower-concentration ammonia only initiate SOD-CAT-GR-G6PDH defense and higher ammonia activated the SOD-CAT-GPx-GSH-GR-G6PDH antioxidant response. In addition, significant increases of serum urea and hepatic ammonia, urea, glutamine, arginase as well as glutamine synthetase were detected with the increase of TA-N (P < 0.05), while serum ammonia levels kept stable (P > 0.05). The present findings further revealed that ammonia could be detoxified directly into glutamine and urea in Wuchang bream to cope with ammonia exposure. In conclusion, under chronic ammonia exposure, enhanced hepatic antioxidant responses as well as increased urea and glutamine synthesis worked in combination to allow Megalobrama amblycephala to defend against environmental ammonia toxicity.
Keywords: Antioxidant response; Detoxification; Glutamine; Oxidative stress; Urea.
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