MG-101

This study comprehensively investigated the effects of different ammonia nitrogen models during transportation on the energy metabolism, redox system, apoptosis, and changes in muscle quality of fish using molecular biology and metabolomics. Exposure to ammonia nitrogen caused intensive stress response as evidenced by alteration on the levels of biochemical indicators (cortisol, glucose, urea nitrogen, alanine transaminase, lactic dehydrogenase, superoxide dismutase, and glutathione peroxidase) and structural disruption of organs (including gill, cephalic kidney, kidney, and liver). As a result of the ammonia nitrogen stress, the redox system became imbalance, leading to disturbance in energy metabolism primarily through the pathways of D-amino acid metabolism, alanine/aspartate/glutamate metabolism, and purine metabolism. Additionally, apoptosis occurred following stress, regulated by FoxO, mTOR, NF-κB, and PI3K/AKT signaling pathways. Besides redox system, energy metabolism, and apoptosis, the change of muscle quality were also influenced by ammonia nitrogen concentration and exposure duration. Drip loss increased with higher ammonia nitrogen concentrations and longer exposure time, while shear force value showed an inverse trend. Although no significant changes were observed in a* and b* values following ammonia nitrogen exposure, the highest W and L* values were found in the low-concentration groups. The correlation of spearman indicates the changes in muscle quality, including drip loss, shear force, and color, induced by ammonia nitrogen during transportation was attributed to the interplay of redox system, energy metabolism, and apoptosis.