Ammonia in aquatic environments is toxic to fish, directly impacting their growth performance and development. Activation of autophagy can facilitate intracellular component renewal and enhance an organism's adaptability to adverse environments. Therefore, this study investigates the impact of autophagy on the yellow catfish under acute ammonia stress. In this study, the yellow catfish intraperitoneally injected with 0.9 % sodium chloride were placed with 0 (CON group) and 125 (HA group) mg/L T-AN (Total ammonia nitrogen) dechlorinated water. The yellow catfish intraperitoneally injected with 30 mg/kg fish CQ (Chloroquine, HA + CQ group) and 1.5 mg/kg fish RAPA (rapamycin, HA + RAPA group) were placed in dechlorinated water containing 125 mg/L T-AN. The results showed that activation of autophagy by injecting with RAPA can alleviate oxidative stress (catalase, superoxide dismutase, total antioxidant capacity significantly increased, H₂O₂ content significantly decreased), and inflammatory response (pro-inflammatory factors TNF-α, MyD88, IL 1-β gene expression decreased significantly), apoptosis (baxa, Bcl2, Tgf-β, Smad2, Caspase3, Caspase 9 gene expression decreased significantly) induced by ammonia stress. In addition, activation of autophagy in yellow catfish can enhance ammonia detoxification by promoting the urea cycle and synthesis of glutamine (the mRNA level of CPS Ⅰ, ARG, OTC, ASS, ASL, and GS increased in the HA + RAPA group). The data above demonstrates that activating autophagy can alleviate oxidative stress, inflammatory responses, and cell apoptosis induced by ammonia stress. Therefore, enhancing autophagy is proposed as a potential strategy to mitigate the detrimental impacts of ammonia stress on yellow catfish.

水生环境中的氨对鱼类有毒，直接影响其生长性能和发育。自噬的激活可以促进细胞内成分更新并增强生物体对不利环境的适应能力。因此，本研究探讨急性氨胁迫下自噬对黄颡鱼的影响。本研究将腹腔注射0.9%氯化钠的黄颡鱼置于0（CON组）和125（HA组）mg/L T-AN（总氨氮）脱氯水中。将腹腔注射30 mg/kg鱼CQ（氯喹，HA+CQ组）和1.5 mg/kg鱼RAPA（雷帕霉素，HA+RAPA组）的黄颡鱼置于含125 mg/L T-AN的脱氯水中。结果显示，注射RAPA激活自噬可减轻氧化应激（过氧化氢酶、超氧化物歧化酶、总抗氧化能力显着升高，H ₂ O ₂含量显着降低）和炎症反应（促炎因子TNF-α、MyD88、氨胁迫诱导IL 1-β基因表达显着下降）、细胞凋亡（baxa、Bcl2、Tgf-β、Smad2、Caspase3、Caspase 9基因表达显着下降）。此外，黄颡鱼自噬的激活可以通过促进尿素循环和谷氨酰胺合成来增强氨解毒（HA+RAPA组中CPSⅠ、ARG、OTC、ASS、ASL和GS的mRNA水平增加）。上述数据表明，激活自噬可以减轻氨应激诱导的氧化应激、炎症反应和细胞凋亡。因此，增强自噬被认为是减轻氨胁迫对黄颡鱼有害影响的潜在策略。