Comprehensive transcriptomic and metabolomic analysis provides insight into transportation stress effects on fish muscle quality
摘要
Transportation, a critical link in the aquaculture industry chain, triggers significant economic losses through stress-induced muscle quality deterioration in fish. This multi-omics study explored the mechanisms underlying transportation stress-induced quality deterioration of fish muscle. Transportation stress elevated cortisol, glucose, lactate dehydrogenase, and oxidative markers (SOD), alongside gill/liver tissue damage. Stress reduced muscle shear force, whiteness, and water-holding capacity, which were highly related to the disruption of muscular structure. Transcriptomics revealed dysregulation of AMPK, PI3K-Akt, FoxO, and MAPK pathways via pfkfb, akt, gadd45, gabarap, jun. Metabolomics highlighted TCA cycle disruption, altered fructose and mannose/pyruvate metabolism, and purine imbalance (e.g., D-mannose 6-phosphate, malate, IMP). Muscle quality parameters negatively correlated with oxidative stress (gpx) and apoptosis (casp3/8/9), but positively linked to DL-glutamine and D-fructose 6-phosphate. Results demonstrate that transportation stress impairs muscle quality via energy dysregulation, oxidative damage, and apoptosis, thus providing a theoretical basis to optimize aquaculture transport and reduce economic losses.