Prolonged low-salinity stress drives coordinated energy metabolism reprogramming and membrane lipid remodeling in the hepatopancreas of mated female mud crab (Scylla paramamosain): An integrated multi-omics study

The mud crab Scylla paramamosain is a commercially important euryhaline crustacean, yet the long-term hepatopancreatic response to low salinity remains largely uncharacterized. Adult mated females were exposed to (30, 15, and 5 ppt) salinity for 40 days, and hepatopancreatic responses were assessed using integrated histological, biochemical, transcriptomic, metabolomic, and lipidomic analyses. Low salinity exposure inhibited growth and survival and caused progressive hepatopancreatic injury, from lumen dilation at 15 ppt to severe vacuolization, basement-membrane disruption, and haemocyte infiltration at 5 ppt. Salinity stress elevated superoxide dismutase activity and reduced malondialdehyde content, whereas total protein declined, suggesting antioxidant activation and protein mobilization to meet energetic demands. Transcriptomic and gene set enrichment analyses showed coordinated activation of oxidative phosphorylation, the tricarboxylic acid cycle, ribosome, and proteasome pathways, together with sustained cytochrome p450 and UDP glucuronosyltransferase mediated detoxification. Steroid biosynthesis was selectively suppressed under low salinity. Metabolomic profiling shifted with salinity level, from nutrient-sensing signaling and amino-acid metabolism at 15 ppt to AMPK and HIF-1 signaling, the tricarboxylic acid cycle, and nucleotide metabolism at 5 ppt. Lipidomic evidence revealed extensive glycerophospholipid and cardiolipin remodeling, linking membrane adaptation with mitochondrial energy metabolism. Integrated analysis identified glycolysis/gluconeogenesis as the only significantly co-enriched pathway at 5 ppt, with pyruvate emerging as a key node linking glycolysis and the TCA cycle in the integrated network. Overall, prolonged low-salinity exposure compromises hepatopancreatic integrity while activating coordinated energy mobilization, membrane remodeling, and detoxification responses that support osmotic adaptation in female mud crabs.