Effects of 1-MCP Treatment on Chilling Injury and ROS Metabolism in Postharvest Passion Fruit

Peel chilling injury severely limits cold storage and long-distance transport of passion fruit, but whether 1-methylcyclopropene (1-MCP) can mitigate this disorder and how it remodels reactive oxygen species (ROS) metabolism remain unclear. In this study, passion fruit were fumigated with 1 μL/L 1-MCP for 24 h at 20 °C and then stored at 4 °C for up to 20 d. Chilling injury index (CII), membrane integrity indicators including relative electrolyte leakage (REL), malondialdehyde (MDA) and carbonyl protein (CP) content, ROS accumulation including hydrogen peroxide (H2O2) and superoxide anion (O2.−), non-enzymatic antioxidants ascorbic acid (AsA) and glutathione (GSH), antioxidant enzyme activities of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) and glutathione reductase (GR), respiration and ethylene production, and transcript abundance of five antioxidant genes (PeSOD1, PeSOD2, PeCAT, PeAPX and PeGR) were monitored. 1-MCP delayed peel degreening and suppressed chilling injury (CI) development, with the CII at 20 d reaching only 62.50% of the untreated control. Compared with the control, 1-MCP reduced REL, MDA and CP accumulation, and lowered H2O2 content and O2.− production rate, with H2O2 at 20 d reaching only 47.46% of the control. 1-MCP also preserved larger AsA and GSH pools, with AsA at 20 d reaching 1.75-fold the control, and sustained higher SOD, CAT, APX and GR activities, with GR and APX at 20 d reaching 3.28-fold and 1.84-fold the control, respectively. These enzyme changes were consistent with the upregulated expression of the corresponding genes. 1-MCP dampened the early rises in respiration and ethylene and maintained higher metabolic activity during late storage. Principal component analysis showed that 1-MCP retarded progression along the first principal component accounting for 51.27% of total variance and strengthened the second principal component accounting for 28.95%. These results suggest that the alleviation of CI by 1-MCP was associated with the coordinated reinforcement of the enzymatic and AsA-GSH antioxidant systems, which may have contributed to the suppression of the ROS burst and the associated membrane lipid and protein oxidation, and to the preservation of membrane integrity and metabolic homeostasis.