Low temperature stress induces tissue-specific metabolic reprogramming and mitochondrial injury in Macrobrachium rosenbergii: Insights from integrated transcriptomic and physiological analyses

Low temperature constitutes a major environmental constraint on the successful cultivation and survival of the giant freshwater prawn, Macrobrachium rosenbergii . However, the physiological mechanisms underlying low temperature-induced tissue damage and metabolic adjustments remain elusive. This study integrated transcriptomics, ultrastructural observation, enzyme activity assays and gene expression analysis to investigate the systemic response of M. rosenbergii muscle and hepatopancreas to low temperature stress. Transcriptomic profiling demonstrated that the identified differentially expressed genes were significantly enriched in several key biological processes, including cellular metabolism, glycolysis/gluconeogenesis, redox homeostasis, and cytochrome P450-mediated detoxification. Transmission electron microscopy revealed severe mitochondrial swelling and dissolution of cristae in the hepatopancreas, whereas muscle ultrastructure remained relatively intact, indicating that the hepatopancreas is the primary target of low-temperature-induced cellular injury. Metabolic analysis indicated muscle tissue significantly upregulated key glycolytic enzymes (Hexokinase, Phosphofructokinase, Lactate dehydrogenase) and Succinate dehydrogenase ( p < 0.05), suggesting a compensatory shift toward anaerobic glycolysis and energy mobilization to maintain function. Conversely, the hepatopancreas exhibited suppressed metabolic enzyme activities and a significant downregulation of antioxidant genes ( CAT , Se-GPx , SOD ), despite the robust upregulation of stress markers ( HSP70 , P450 ), suggesting the activation of defense mechanisms in response to oxidative damage. These results are highly consistent with the transcriptomic data. Overall, short-term low temperature stress increases reliance on anaerobic metabolism through metabolic reprogramming and disrupts mitochondrial function, thereby inducing oxidative stress and activating the anti-stress response. This study elucidates the mechanisms of early low temperature adaptation and injury in M. rosenbergii from a metabolic perspective, providing a theoretical basis for developing low temperature aquaculture management strategies and screening physiological biomarkers for low temperature resistance.