Abstract
The effect of postharvest heat treatment (37 °C, 3 days) on ascorbic acid (AsA) metabolism related to chilling resistance in peach fruit stored at 5 °C has been studied. Chilling injury (CI) index and hydrogen peroxide (H2O2) levels as well as gene expression levels of mitochondrial L-galactono-1, 4-lactone-dehydrogenase (GalLDH) related to AsA synthetic metabolism, cytosolic ascorbate peroxidase (APX), chloroplastic APX, peroxisomal APX1-3, cytosolic monodehydroascorbate reductase (MDAR), chloroplastic MDAR, chloroplastic dehydroascorbate reductase (DHAR), and chloroplastic glutathione reductase (GR) related to AsA regeneration cycle metabolism were measured. Treated fruit maintained its initial H2O2 levels after heat conditioning, showing significantly higher levels when compared with non-heated fruit. However, during cold storage, heat-treated fruit exhibited lower H2O2 levels than control fruit; heated fruit had the lowest CI index at the end of storage. The transcription levels of all of genes (GalLDH, APX, MDAR, and DHAR), except for GR, sharply increased, and were higher than those of control fruit, immediately after heat treatment. Then, transcription levels sharply declined to levels lower than control fruit at 7–14 days. Little difference of gene expression was observed in the end of storage. These results suggest that AsA metabolism gene expression was temporarily and sharply induced by higher H2O2 levels after heat treatment, which might inhibit the elevation of H2O2 level at the initial period of cold storage, and followed by lower genes expression of AsA metabolism accompanied by lower H2O2 levels following transfer to cold storage.
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