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Chilling‐related cell damage of apple ( Malus × domestica Borkh.) fruit cortical tissue impacts antioxidant, lipid and phenolic metabolism
Author(s) -
Leisso Rachel S.,
Buchanan David A.,
Lee Jinwook,
Mattheis James P.,
Sater Chris,
Hanrahan Ines,
Watkins Christopher B.,
Gapper Nigel,
Johnston Jason W.,
Schaffer Robert J.,
Hertog Maarten L.A.T.M.,
Nicolaï Bart M.,
Rudell David R.
Publication year - 2015
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/ppl.12244
Subject(s) - malus , metabolite , biochemistry , phytosterol , metabolism , chemistry , antioxidant , lipid metabolism , metabolomics , catechin , biology , food science , botany , polyphenol , chromatography
‘Soggy breakdown’ (SB) is an internal flesh disorder of ‘Honeycrisp’ apple ( Malus × domestica Borkh.) fruit that occurs during low temperature storage. The disorder is a chilling injury (CI) in which visible symptoms typically appear after several weeks of storage, but information about the underlying metabolism associated with its induction and development is lacking. The metabolic profile of flesh tissue from wholly healthy fruit and brown and healthy tissues from fruit with SB was characterized using gas chromatography‐mass spectrometry (GC‐MS) and liquid chromatograph‐mass spectrometry (LC‐MS). Partial least squares discriminant analysis (PLS‐DA) and correlation networks revealed correlation among ester volatile compounds by composition and differences in phytosterol, phenolic and putative triacylglycerides (TAGs) metabolism among the tissues. anova ‐simultaneous component analysis (ASCA) was used to test the significance of metabolic changes linked with tissue health status. ASCA‐significant components included antioxidant compounds, TAGs, and phytosterol conjugates. Relative to entirely healthy tissues, elevated metabolite levels in symptomatic tissue included γ‐amino butyric acid, glycerol, sitosteryl (6′‐O‐palmitoyl) β‐ d ‐glucoside and sitosteryl (6′‐O‐stearate) β‐ d ‐glucoside, and TAGs containing combinations of 16:0, 18:3, 18:2 and 18:1 fatty acids. Reduced metabolite levels in SB tissue included 5‐caffeoyl quinate, β‐carotene, catechin, epicatechin, α‐tocopherol, violaxanthin and sitosteryl β‐ d glucoside. Pathway analysis indicated aspects of primary metabolism differed according to tissue condition, although differences in metabolites involved were more subtle than those of some secondary metabolites. The results implicate oxidative stress and membrane disruption processes in SB development and constitute a diagnostic metabolic profile for the disorder.

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