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  • Author or Editor: George D. Nanos x
  • Journal of the American Society for Horticultural Science x
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`Bartlett' pears (Pyrus communis L.) at two physiological stages, climacteric minimum or approaching the climacteric peak as achieved via storage for 2 or 8 weeks in air at 0C, respectively, were either ripened at 20C in air immediately or after exposure to 0.25% 02 for 4 days at 20C. Fruit stored for 2 weeks had relatively stable phosphofructokinase (PFK), pyrophosphate: fru-6-P phosphotransferase (PFP), and pyruvate kinase (PK) activities but decreasing succinate dehydrogenase (SDH) activities during ripening in air. Similar fruit treated with 0.25% O2 had slightly increased PFK, PFP, and SDH activities and decreased PK activity. Fruit stored for 8 weeks exhibited higher levels of PFK and PFP activity upon transfer to 20C, in accordance with their more advanced physiological state. In general, the enzymic changes in these fruit upon exposure to 0.25% O2 and subsequent ripening in air were similar to those observed in the less-mature counterparts, most notable being an increase in mitochondrial SDH. Exposure of suspension-cultured pear fruit cells to hypoxia resulted in an accentuated rise in phosphoenolpyruvate carboxykinase activity and a dramatic rise in SDH activity upon transfer to air. Taken in concert, the enzymic analysis supports the hypothesis that the rise in succinate levels observed in hypoxic fruit tissues is the result of a partial reductive tricarboxylic acid cycle. Cytochrome oxidase activity did not change during hypoxia whereas soluble peroxidase decreased somewhat, perhaps a reflection of their Michaelis constants for O2.

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`Bartlett' pears (Pyrus communis L.) that had been stored for either 2 or 8 weeks in air at 0C were placed under an atmosphere of 0.25% 0, (balance N2) at 20C for 4 days then returned to air. Control pears were kept in air at 20C. Suspension-cultured `Passe Crassane' pear fruit cells in aging medium were treated similarly. During exposure of the fruit to 0.25% O2, loss of greenness and ethylene production were inhibited and CO2 production substantially decreased. Pears that had been stored for 2 weeks at 0C ripened normally, while those that had been stored for 8 weeks at 0C failed to recover normal ethylene and CO2 production upon transfer to air after a 4-day exposure to 0.25% O2 at 20C. Most of the latter fruit were injured as indicated by skin browning. Acetaldehyde and ethanol content increased considerably with ripening of control fruit. Although 0.25% O2-treated fruit developed yet higher acetaldehyde and ethanol contents during treatment, the concentrations returned to or below normal during subsequent exposure to air. Pears exposed to 0.25% 0, had increased pyruvate decarboxylase (PDC; EC 4.1.1.1) and alcohol dehydrogenase (ADH; EC 1.1.1.1) activities that remained high after ripening in air for 6 days. Three ADH isozymes were discernible in the 0.25% O2-treated pears, whereas only one, ADHZ, was found in control fruit. These observations imply that preclimacteric pears are both less stressed during hypoxia and have greater potential for posthypoxia repair than pears of a more advanced physiological age. Increased posthypoxia respiratory and enzymatic activity and the elaboration of new ADH isoenzymes appear to be part of the repair response. Suspension-cultured pear fruit cells responded to the atmospheric changes very much like the S-week stored fruit and likely is a good model system to further study the effects of hypoxia on pear metabolism.

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