Ammonia-N is a common toxic factor in aquatic environment, known to inhibit fish feeding, yet its mechanism remains unclear. To investigate the toxicological mechanism of ammonia-N in inhibiting fish feeding, this study conducted experiments exposing juvenile Siberian sturgeon (Acipenser baerii) to ammonia-N at concentrations of 0, 5, 10, and 15 mg/L for 14 days. The results revealed a significant reduction in both daily and cumulative food intake. Obviously decreased condition factor (CF), hepatosomatic index (HSI), and viscerosomatic index (VSI) at 15 mg/L (P < 0.05). Besides, the serum ammonia concentration significantly increased on the 14th day, while the neurotoxic marker acetylcholinesterase (AchE) showed a consistent increase over the 14-day period (P < 0.05). Pathological examination of brain tissue demonstrated that ammonia-N induced damage, particularly evident in 15 mg/L ammonia-N group, where severe nerve fiber dissolution was observed. Moreover, the activity of superoxide dismutase (SOD) was significantly increased in the brain on the 1st, 3rd, and 7th day (P < 0.05). RNA-seq analysis o revealed 1566, 2188, and 2026 differentially expressed genes (DEGs) were obtained in the 5, 10, and 15 mg/L ammonia-N groups, respectively, compared to the control group, and 30 DEGs related to appetite regulation were identified. Further quantitative real-time PCR (qPCR) analysis indicated that ammonia-N exposure changed the expressions of appetite factors, including downregulation of agouti-related protein (agrp) and neuropeptide Y (npy), and upregulation of pro-opiomelanocortin (pomc), cocaine-and amphetamine-regulated transcript peptide (cart), and corticotropin releasing factor (crf) (P < 0.05). Therefore, these results suggest that ammonia-N inhibits feeding via neurotoxicity induced oxidative damage which primarily by downregulating appetite promoting factors and upregulating appetite-inhibiting factors. This study lays the groundwork for deeper understanding of the toxicological mechanism of ammonia-N on aquatic animals, particularly its detrimental effects on fish brain function and feeding behavior.
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