Cell wall disassembly and post-harvest deterioration of ‘sweetheart’ sweet cherry fruit: involvement of enzymic and non-enzymic factors
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Sweet cherries are very perishable, owing to rapid softening rates associated to significant deterioration of fruit. Ripening-related firmness loss is generally attributed to enzyme-catalysed modifications in cell wall composition and structure, but some experimental evidence suggests that non-enzymic
mechanisms may be also involved in the process. In this study, 'Sweet Heart' cherries were picked at commercial maturity and kept at 0 ºC during 15 or 30 days, followed by up to 3 days at 20 ºC to simulate commercial shelf life. Cell wall materials were extracted, fractionated and analysed, and some cell wall-modifying enzyme activities were assessed for a possible role on firmness loss and overall deterioration of fruit. Radical scavenging activity (RSA) and both reduced and oxidised ascorbate contents were also analysed in each case. Regression analysis revealed that firmness was associated to reduced ascorbate and RSA, in turn inversely correlated to decay and weight loss. Higher firmness levels were found for fruit displaying higher RSA and yields of the cell wall fractions containing covalently-bound pectins and hemicelluloses, while decay correlated inversely with RSA and reduced ascorbate content. Polygalacturonase (PG) and pectate lyase (PL) activities were related to solubilisation of cell wall pectins and inversely to reduced ascorbate, but not to firmness-contributing cell wall fractions, which correlated rather to enzyme activities acting on pectin side-chains that control the access to substrates of backbone-degrading enzymes. Data suggest that antioxidant status may play a major role in modulating cell wall disassembly of sweet cherry fruit.