Abstract

Controlled atmosphere (CA) storage limits ethylene-related ripening of apple fruit, but can promote the development of CA-related injury. CA-related injury can be exacerbated by the ethylene antagonist, 1-methylcyclopropene (1-MCP). The main objective of this study was to investigate the impact of pre-storage conditioning, 1-MCP and elevated CO2 on the development of CA-related injury and oxidative stress metabolites in ‘Honeycrisp’ (Malus×domestica Borkh.) apple fruit. Upon harvest, fruit were treated with or without 1μLL−1 1-MCP for 24h, and then transferred to CA (2.5kPa O2 and 2.5kPa or 0.03kPa CO2) at 3°C (no conditioning) or conditioned at 10°C for 5d prior to CA. Apples were CA-stored for up to 35 weeks. CA-related injury occurred with storage under both CA regimes, regardless of 1-MCP and conditioning, whereas 1-MCP exacerbated the negative impact of elevated CO2 on this disorder, approximating an 80% incidence, which was coincident with a 400% increase in γ-aminobutyrate (GABA). By comparison, pre-storage conditioning reduced the negative impact of 1-MCP on the incidence of CA-related injury at 2.5kPa CO2 by nearly 80%, and this was associated with a dramatically lower GABA concentration. Overall, rapid declines in total ascorbate and ascorbate/dehydroascorbate ratios were evident with storage, regardless of treatment. Transient declines in total glutathione and glutathione/glutathione disulphide ratios were more rapid and sustained for longer periods of time in conditioned than non-conditioned fruit. There were dramatic shifts in the levels of phosphorylated and non-phosphorylated pyridine dinucleotides with storage duration, regardless of treatment, resulting in elevated ratios of NADPH/NADP+ and NADH/NAD+ after 35 weeks, especially for conditioned fruit subjected to elevated CO2. Canonical powered partial least squares analysis revealed that metabolite profiles changed with storage period and treatment, and were most divergent during elevated CO2 storage. Moreover, CA-related injury was strongly associated with changes in GABA, and moderately linked to total glutathione and glutathione redox status.

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