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Abstract
My aim in this brief presentation is to illustrate how the interplay of senescence and homoeostasis can offer a context within which to question and, in part, explain various postharvest phenomena. I should like to begin by briefly noting the status of principal phenomena and related paradigms that have influenced postharvest research, namely the respiratory climacteric, ethylene, and molecular (genetic) determinants.
A strong association is implicit between mitochondrial function and the energy demands of cells responding to stress. Yet, the dynamics of this organelle-cellular dependency have been difficult to resolve. This study examines a new diagnostic parameter namely, mitochondrial maintenance and self-restoration as exhibited by the course of respiratory functions (states 3 and 4 respiratory rates, respiratory control) of mitochoudria extracted during and after exposure of intact `Hass' avocado (Persea americana) fruit to different stress atmospheres: anoxia (100% N2) or high (25% and 75%) CO2 for varying durations. Comparisons are made with direct exposure of the mitochondria themselves to similar atmospheres. In general, exposure of the fruit to CO2 rich atmospheres enhanced the capacity of their mitochondria to restore energy-linked functions whereas anoxia caused irreparable damage. The physiological (climacteric) state of the fruit also affected the stress capacity of the mitochondria contained therein, anaerobiosis being more harmful to mitochondria in riper fruit. In contrast to their effects in vivo, in vitro anoxia appeared to sustain mitochondrial energy-linked functions, whereas high CO2 was clearly harmful. These and other observations are discussed in the context of mitochondrial self-restoration or homeostasis and its relevance to postharvest stress-atmosphere storage for purposes such as pathogen suppression or insect control.
The response of pear fruits and suspension-cultured pear fruit cells to 0% or 0.25% O2 is being examined to evaluate the feasibility of using such atmospheres for postharvest insect control. These treatments inhibited ethylene production, had no effect on acetaldehyde content, and increased ethanol production in pears kept at 20C for 10 days. The blossom end area of pear fruits was more prone to anaerobiosis, as indicated by increased alcohol dehydrogenase activity and ethanol content. Pear fruit plugs showed increased respiration and ethylene production rates when skin was present compared to plugs without skin. Methods for measuring activity of alcohol dehydrogenase, pyruvate decarboxylase, and pyruvate kinase have been modified and optimized and will be used to determine changes in pear fruit tissue during low O2 treatment and subsequent recovery in air.
Abstract
Application of 400 ppm aminoethoxyvinylglycine (AVG) to pear trees 6 and 2 weeks before harvest resulted in marked but variable inhibition of postharvest ripening at 20°C. AVG amplified the usual nonuniformity in the initiation of ripening exhibited by freshly harvested fruit. Prolonged storage of the fruit at 0 to 2°c counteracted the inhibitory effects with resultant rapid and uniform ripening upon transfer to 20°c. However, a physiological nonuniformity as reflected by wide differences in internal C2H4 concentration persisted well beyond the time when threshold levels for the initiation of ripening had been reached by all fruit. Probable relationships between AVG effects, cold storage, and C2H4 are illustrated diagrammatically.
`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.
Abstract
Preharvest treatment with 400 ppm aminoethoxyvinylglycine (AVG) delayed the ripening of ‘Bartlett’ pears kept at 20°C. The effect was not uniform, with the delay in ripening ranging from a few to 112 days. Prolonged storage at 20° was accompanied by a relatively steady, low level of respiration, gradual degreening, and partial suppression of the eventual climacteric. The combined effect of AVG treatment and prolonged ‘nonripening’ storage at 20° led to a marked attentuation of the production of 4 readily measurable volatiles including methyl-, ethyl-, and hexylacetate as identified by cochromatography and combined gas chromatography–mass spectrometry. Surprisingly, prolonged storage resulted in a much increased production of 2 other volatile fractions when AVG inhibition was reversed by C2H4 treatment. The emanation of all measured volatiles was closely coincident with the climacteric peak. These observations confirm prior reports of disuniform effects of preharvest AVG treatment and reveal that metabolic transitions during prolonged, nonripening storage may have adverse effects on fruit quality.
Suspension-cultured `Passe Crassane' pear fruit (Pyrus communis L.) cells in aging media were ventilated with air or air + 20% CO2 for 4 days at 26C. Cells exposed to elevated CO2 exhibited reduced respiration (02 consumption). Ethylene production of both air and CO2-treated cells also declined to barely discernible levels by day 3. Fructose 6-phosphate (F6P) accumulated, while levels of fructose l,6-bisphosphate (F1, 6-P2), and activities of ATP and PPi phosphofructokinases (PFK and PFP) declined in response to elevated CO2. These results indicate an inhibitory effect of CO2 at the site of action of both phosphofructokinases in the glycolytic pathway, which could account, at least in part, for the observed reduction in respiration. The responses to elevated CO2 levels of the cell suspension system and intact pear fruit ventilated with air + 10% CO2 are compared, revealing a close similarity.
Abstract
The extinction point (EP), defined as the lowest O2 concentration at which alcohol production ceases, was a useful concept in early interpretations of the Pasteur effect in fruit. However, ethanol is now known to be a normal constituent of many fruits under aerobic conditions. Therefore, we propose an alternative concept, the anaerobic compensation point (ACP), defined as the O2 concentration at which CO2 evolution is minimum. After 2 to 4 hr under various O2 concentrations, the ACPs of mature-green pears (Pyrus communis L.) and pear cell cultures are 1.6% to 1.7% and 1.1% to 1.3% O2, respectively. The ACP shifts to lower O2 concentrations upon extended exposure of the cells to low-O2 atmospheres and to higher O2 concentrations as pear fruit mature physiologically or as the diffusion coefficient of cell suspensions is decreased. With O2 diffusion coefficients of 4.4, 3.7, and 2.5 × 10−6 cm2·s−1, the ACP effect is observed just below 1.3%, 3.0%, and 5.0% O2, respectively. Analogies between the responses of intact fruit and suspension-cultured cells to limiting O2 are illustrated and use of the latter in assessing the response of pear cells to changing coefficients of diffusion is discussed.
`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.