Abstract

In order to evaluate the effect of ethanol vapor treatments (0.5mL/kg and 3mL/kg) on postharvest storage at 23°C, quality of oriental sweet melons, and to clarify the mechanism of the inhibition of senescence, we investigated physiological and quality changes induced by ethanol vapor, decay incidence, internal ethylene concentration (IEC) and ethylene-related enzymes activities as well as gene expression. Both ethanol vapor treatments, irrespective of concentration, significantly (P<0.5) delayed skin color changes, retarded softening and suppressed fruit decay in ethanol vapor-treated fruit. Between the two treatments, 0.5mL/kg of ethanol vapor maintained better quality in storage than that of 3mL/kg. Compared with the control, both ethanol vapor treatments resulted in different profiles and composition of aromatic volatile compounds of fruit during storage, and a significant increase of ethyl esters, including ethyl acetate, ethyl butanoate, ethyl hexanoate, ethyl 2-methylbutanoate, 3-(methylthio) propionate and 2-phenethyl acetate, and five new ethyl esters were also detected. Both treatments increased alcohol acyl-transferase (AAT) activity levels, which peaked earlier than in the control, but there were no significant differences in activities of alcohol dehydrogenase (ADH). Both treatments significantly (P<0.5) suppressed internal ethylene concentrations (IEC) during storage at 23°C, which was evident from reducing 1-aminocyclopropane-1-carboxylic acid (ACC) synthase (ACS) and ACC oxidase (ACO) activities, and inhibiting ACC biosynthesis, and the effect of the 0.5mL/kg treatment was better than that of 3mL/kg. Real-time quantitative PCR (Q-PCR) analysis showed that the expression patterns of CM-ACO1, CM-ACO2, CM-ACS1 and CM-ACS2 were consistent with ethylene production during storage. These results suggest that postharvest ethanol vapor treatments markedly delayed the senescence of harvested oriental sweet melons, maintained better quality in storage and improved levels of volatile aroma compounds, especially the ethyl esters, through suppressing the expression of particular members of ethylene-forming enzyme gene families as well as ethylene biosynthesis, and the effect is dose dependent.

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