Elevated environmental ammonia leads to respiratory disorders and metabolic dysfunction in most fish species, and the majority of research has concentrated on fish behavior and gill function. Prior studies have rarely shown the molecular mechanism of the largemouth bass hepatic response to ammonia loading. In this experiment, 120 largemouth bass were exposed to total ammonia nitrogen of 0 mg/L or 13 mg/L for 3 and 7 days, respectively. Histological study indicated that ammonia exposure severely damaged fish liver structure, accompanied by increased serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase activity. RT-qPCR results showed that ammonia exposure down-regulated the expression of genes involved in glycogen metabolism, tricarboxylic acid cycle, lipid metabolism, and urea cycle pathways, whereas it up-regulated the expression of genes involved in gluconeogenesis and glutamine synthesis pathways. Thus, ammonia was mainly converted to glutamine in the largemouth bass liver during ammonia stress, which was rarely further used for urea synthesis. Additionally, transcriptome results showed that ammonia exposure also led to the up-regulation of the oxidative phosphorylation pathway and down-regulation of the mitogen-activated protein kinase signaling pathway in the liver of largemouth bass. It is possible that the energy supply of oxidative phosphorylation in the largemouth bass liver was increased during ammonia exposure, which was mediated by the MAPK signaling pathway.
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