Melatonin mobilizes the metabolism of sugars, ascorbic acid and amino acids to cope with chilling injury in postharvest pear fruit

Chilling injury manifesting as internal browning is an irreversible physiological disorder in cold-stored 'Yali' pear fruit, which seriously restricts postharvest handling and commercialization of pear fruit. This study investigated the impact of melatonin (MN) treatment on chilling injury and the metabolism of sugars, ascorbic acid (AsA), proline, and gamma-aminobutyric acid (GABA) during chilling injury development in 'Yali' pears. The findings revealed that MN-treated pear fruit exhibited considerably improved tolerance to chilling stress compared with untreated control fruit. MN application augmented proline accumulation, likely owing to increased activities and transcriptional concentrations of Delta(1)-pyrroline-5-carboxylate synthase and ornithine-delta-aminotransferase as well as diminished activity and transcriptional level of proline dehydrogenase. MN immersion increased enzyme activities and gene expression related to the GABA shunt pathway, leading to increased GABA concentrations in cold-stored pear fruit. Furthermore, MN treatment elevated AsA concentrations in the fruit, exerting protective effects against cell membrane damage and mitigating oxidative stress damage caused by chilling. Compared with the control group, MN-treated fruit exhibited reduced neutral invertase enzyme activity and gene expression. Additionally, MN treatment increased both sucrose-phosphate synthase and sucrose synthase activities and gene expression in pear fruit. These observations indicated that the enhanced chilling tolerance of 'Yali' pear fruit following MN treatment may be associated with the regulation of proline, GABA, AsA, and soluble sugars metabolism.