Peach fruit faces severe postharvest losses due to thin epidermis and susceptibility to Rhizopus stolonifer-induced soft rot. Chemical control risks residue and resistance issues, demanding eco-friendly alternatives. This study elucidated the mechanism by which trans-2-hexenal (E2H) mitigated postharvest soft rot caused by Rhizopus stolonifer in peach (Prunus persica cv. Hujing Milu) fruit. The results demonstrated that E2H treatment significantly delayed lesion expansion by 44.7% and disease incidence by 23.9% while effectively maintaining fruit quality by delaying firmness loss, reducing juice leakage, and suppressing malondialdehyde (MDA) accumulation. E2H treatment upregulated phenylpropanoid pathway gene expression, enhancing key phenylpropanoid metabolism enzymes activities (phenylalanine ammonia-lyase (PAL), cinnamate 4-hydroxylase (C4H), 4-coumarate-CoA ligase (4CL), polyphenol oxidase (PPO), peroxidase (POD)), leading to the increase of total phenolics by 7.9%. E2H treatment analysis revealed significant enhancements in both chitinolytic activity (CHI) and β-1,3-glucanase (GLU) activity by 85.7% and 12.9%, indicating potentiation of the enzymatic defense system. Concurrently, E2H treatment could improve the redox modulation capacity of peach fruits through promoting catalytic efficiency of redox-regulating enzymes, increasing the accumulation of ascorbic acid (AsA) by 8.1%, inhibiting the synthesis of dehydroascorbic acid (DHA) by 18.6%, as well as suppressing the biosynthesis of reactive oxygen species (ROS). These coordinated enhancements in pathogenesis-related proteins (CHI, GLU), phenylpropanoid metabolism activation, and antioxidant systems are strongly associated with E2H-induced resistance against Rhizopus stolonifer, though contributions from other factors may also be involved.
Keywords: Rhizopus rot; antioxidant defense; pathogenesis-related proteins (PRs); phenylpropanoid metabolism; trans-2-hexenal.