Investigation of ascorbate metabolism during inducement of storage disorders in pear

In pear and apple, depletion of ascorbate has previously been associated with development of stress‐related flesh browning. This disorder occurs in intact fruit and differs from browning associated with tissue maceration and processing. We investigated changes in ascorbate content, ascorbate peroxidase (APX) activities and gene expression of l‐galactose pathway genes, ascorbate recycling genes and APXs from harvest to 30 days storage for three pear varieties [‘Williams Bon Chretien’ (WBC), ‘Doyenne du Comice’ and ‘Beurre Bosc’]. The pears were stored at 0.5°C in air or controlled atmosphere (CA, 2 kPa O2 and 5 kPa CO2). Storage in CA caused significant amounts of storage disorders in WBC only. Ascorbate content generally declined after harvest, although a transient increase in ascorbate in the form of dehydroascorbate (DHA) between harvest and 3 days was observed in CA stored WBC, possibly due to low at‐harvest monodehydroascorbate reductase and CA‐decreased dehydroascorbate reductase expression. Quantitative polymerase chain reaction indicated that all cultivars responded to CA storage by increasing transcripts for APXs, and surprisingly the pre‐l‐galactose pathway gene GDP‐mannose pyrophosphorylase, of which the product GDP mannose, is utilized either for cell wall polysaccharides, protein N‐glycosylation or ascorbate production. Overall, the small differences in ascorbate we observed suggest how ascorbate is utilized, rather than ascorbate content, determines the potential to develop internal browning. Moreover, a transitory increase in DHA postharvest may indicate that fruits are at risk of developing the disorder.