Transcriptomic and metabolomic profiling reveal the mechanism underlying the inhibition of wound healing by ascorbic acid in fresh-cut potato

•Ascorbic acid (AsA) treatment inhibited StGST but enhanced StPHO1 and StLOX5 gene expression.•AsA-treated samples had higher levels of starch content and starch metabolism.•AsA treatment increased amylase and lipoxygenase activity.•AsA treatment inhibited sucrose degradation and fatty acid synthesis. Ascorbic acid (AsA) inhibits wound healing in fresh-cut potatoes (FCP); however, the comprehensive regulatory mechanisms of the chemical during wound healing remain unclear. Here, physiobiochemical, transcriptomic, and metabolomic analyses were performed. In total, 685 differentially expressed genes (DEGs) and 1921 differentially accumulated metabolites (DAMs) were identified between control and AsA-treated samples. The level of the majority of DEGs expression and DAMs abundance in AsA-treated samples were similar to data of newly cut samples. The collective data indicated that the AsA treatment inhibited wound healing in FCPs by regulating glutathione metabolism, enhancing starch metabolism, and inhibiting phenylalanine metabolism, sucrose degradation, and fatty acid synthesis. Major genes and metabolites affected by AsA treatment included StGST, StPAL, StPHO1 and StLOX5, and starch, sucrose, and linoleic acid. AsA treatment increased starch content and amylase and lipoxygenase activity and decreased free fatty acid level. Our research provides fundamental insights into wound healing mechanisms in FCP.