Abstract：
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.
摘要：
环境氨升高会导致大多数鱼类的呼吸系统疾病和代谢功能障碍，大部分研究都集中在鱼类的行为和ill功能上。先前的研究很少显示大嘴鲈鱼肝脏对氨负荷反应的分子机制。在这个实验中,120大嘴鲈鱼暴露于0mg/L或13mg/L的总氨氮中3天和7天，分别。组织学研究表明，氨暴露严重损害鱼肝结构，伴有血清丙氨酸转氨酶升高，天冬氨酸转氨酶,和碱性磷酸酶活性。RT-qPCR结果显示氨暴露下调糖原代谢相关基因的表达,三羧酸循环，脂质代谢，和尿素循环途径，而它上调了参与糖异生和谷氨酰胺合成途径的基因的表达。因此，氨胁迫期间，大嘴鲈鱼肝脏中的氨主要转化为谷氨酰胺，很少进一步用于尿素合成。此外,转录组结果表明，氨暴露还导致大口鲈鱼肝脏氧化磷酸化途径的上调和丝裂原活化蛋白激酶信号通路的下调。在氨暴露期间，大嘴鲈鱼肝脏中氧化磷酸化的能量供应可能增加，由MAPK信号通路介导。
