Sulfur-release paper treatment delays longan pericarp browning involving flavonoid branch remodeling and the attenuation of enzymatic oxidation.

Pericarp browning is a major factor limiting the postharvest quality and commercial circulation of longan fruit. Although SO₂-releasing paper (SRP) effectively delays browning, its underlying regulatory mechanism remains unclear. In this study, physiological analyses, transcriptomic sequencing, and flavonoid metabolomics were integrated to elucidate SRP-induced delays in longan pericarp postharvest browning. SRP treatment significantly retarded browning progression, maintained a higher total antioxidant activity and total flavonoid content, and suppressed polyphenol oxidase (PPO), peroxidase (POD), and laccase (LAC) activities during storage. Transcriptomic analysis revealed that SRP-responsive genes were mainly enriched in phenylpropanoid metabolism, flavonoid biosynthesis, and redox-related pathways, with four browning-associated oxidative genes (DlLAC7, DlLAC14, DlPOD, and DlPOD2) consistently downregulated under SRP treatment. Metabolomic analysis further revealed pronounced branch-level flavonoid remodeling, characterized by enhancement of the flavonol branch and rebalancing of the flavan-3-ol branch. In particular, flavonol metabolism showed a preferential enrichment of the quercetin-associated branch, with quercetin and kaempferol levels at 50 d being approximately 14.6- and 5.7-fold higher in SRP-treated pericarp than in the control group, respectively; while key flavan-3-ol metabolites, especially (-)-epicatechin, were better preserved under SRP treatment. In vitro enzymatic browning analysis further showed the strongest browning susceptibility for (-)-epicatechin among the tested flavonoid substrates. These results suggest that SRP-delayed longan pericarp browning is associated with the coordinated attenuation of enzymatic oxidation and branch-level flavonoid remodeling, which may help maintain antioxidant capacity.