Postharvest ASM dipping and DPI pre-treatment regulated reactive oxygen species metabolism in muskmelon (Cucumis melo L.) fruit

• ASM dipping decreased lesion diameters on muskmelon fruit inoculated with Trichothecium roseum.
• ASM induced metabolism of reactive oxygen species (ROS) in fruit.
• DPI pretreatment inhibited ROS metabolism and increased lesion development.

Pink rot caused by Trichothecium roseum is one of the most important postharvest diseases of muskmelon. The present study was to evaluate how disease resistance in muskmelon fruit (Cucumis melo L. cv. Yujingxiang) was affected by dipping with 100 mg/L acibenzolar-S-methyl (ASM) and 50 μM diphenylene iodonium (DPI), a NADPH oxidase specific inhibitor. Lesion diameters on the fruit inoculated with T. roseum were significantly decreased (P < 0.05) by dipping with 100 mg/L ASM. Decreased lesion development was associated with the accumulation of H2O2, release of superoxide anion (O2−), enhancement activities of NADPH oxidase (NOX), superoxide dismutase (SOD), ascorbate peroxidase (APX), and inhibition of catalase (CAT) activity. Antioxidant content including ascorbic acid (AsA) and reduced glutathione (GSH) was also induced by ASM treatment. Compared with ASM treated fruit, fruit treated with DPI prior to ASM treatment exhibited larger lesion diameter. Moreover, DPI treatment inhibited ASM-induced H2O2 and O2− accumulation, the increase of NOX, SOD, APX activities and content of ascorbic acid (AsA), and reduced glutathione (GSH). Cytochemical studies indicated that H2O2 and O2− were mainly deposited in the intercellular space and cell walls. These results suggest that pre-treatment with DPI prevented accumulation of ROS induced by ASM and resulted in serious disease symptoms, highlighting the important role of ROS in ASM-induced resistance in muskmelon fruit.