Details
Originalsprache | Englisch |
---|---|
Seiten (von - bis) | 119-128 |
Seitenumfang | 10 |
Fachzeitschrift | Postharvest Biology and Technology |
Jahrgang | 137 |
Frühes Online-Datum | 1 Dez. 2017 |
Publikationsstatus | Veröffentlicht - März 2018 |
Abstract
Skin shrivelling of sweet cherry (Prunus avium L.), referred to here as ‘orange-peel’ disorder, compromises fruit appearance and thus market value. The objectives were to establish a protocol to describe and quantify orange peel disorder and to identify the mechanism and factors determining its incidence. Fruit was stored for 28 to 33 d at 2 °C and 76% RH and orange peel disorder was quantified as a topographical roughness using an interferometer or by rating the fruit for orange peel using a four-step scoring scheme. Fruit with orange peel disorder had a skin topography similar to that of a citrus fruit − just on a finer scale. Under the conditions of the test, orange peel was first visible after ∼7 d and continued to increase in severity thereafter. Orange peel was most severe on the shoulder and in the equatorial and distal regions of the fruit. There was no relationship between the distribution of orange peel and that of stomata or of microcracking. At a microscopic level, the depressions in the fruit surface were markedly larger than the periclinal areas of individual epidermal cells, but similar in size to the mesh formed by the network of minor veins visible just beneath the skin. Susceptibility to orange peel differed among cultivars. Least susceptible were ‘Dönissens Gelbe’ and, ‘Gil Peck’, intermediate were ‘Sam’, ‘Kordia’, ‘Merchant’, and the sour cherry ‘Ungarische Traubige’, and most susceptible were ‘Adriana’, ‘Regina’, and ‘Hedelfinger’. Incidence of orange peel during storage was negatively related to relative humidity (more at lower humidities) but also developed at 100% RH in the absence of transpiration. Submerging fruit in water for 2 d partly reversed orange peel. There was no significant difference in the permeance of the skins or in turgors of cells of the outer mesocarp between fruit without and with orange peel. There was a significant difference between the osmotic potential of the flesh (more negative) and that of the skin (less negative). During storage, the osmotic potentials of flesh and skin both decreased slightly, but the difference between them remained constant. The results show water loss from the skin is causal in orange peel disorder. The water loss from the skin occurs both by two routes: (1) transpiration to the atmosphere and also (2) by osmotic dehydration to the flesh.
ASJC Scopus Sachgebiete
- Agrar- und Biowissenschaften (insg.)
- Lebensmittelwissenschaften
- Agrar- und Biowissenschaften (insg.)
- Agronomie und Nutzpflanzenwissenschaften
- Agrar- und Biowissenschaften (insg.)
- Gartenbau
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in: Postharvest Biology and Technology, Jahrgang 137, 03.2018, S. 119-128.
Publikation: Beitrag in Fachzeitschrift › Artikel › Forschung › Peer-Review
}
TY - JOUR
T1 - Orange peel disorder in sweet cherry
T2 - Mechanism and triggers
AU - Schlegel, Henrik Jürgen
AU - Grimm, Eckhard
AU - Winkler, Andreas
AU - Knoche, Moritz
N1 - © 2017 Elsevier B.V. All rights reserved.
PY - 2018/3
Y1 - 2018/3
N2 - Skin shrivelling of sweet cherry (Prunus avium L.), referred to here as ‘orange-peel’ disorder, compromises fruit appearance and thus market value. The objectives were to establish a protocol to describe and quantify orange peel disorder and to identify the mechanism and factors determining its incidence. Fruit was stored for 28 to 33 d at 2 °C and 76% RH and orange peel disorder was quantified as a topographical roughness using an interferometer or by rating the fruit for orange peel using a four-step scoring scheme. Fruit with orange peel disorder had a skin topography similar to that of a citrus fruit − just on a finer scale. Under the conditions of the test, orange peel was first visible after ∼7 d and continued to increase in severity thereafter. Orange peel was most severe on the shoulder and in the equatorial and distal regions of the fruit. There was no relationship between the distribution of orange peel and that of stomata or of microcracking. At a microscopic level, the depressions in the fruit surface were markedly larger than the periclinal areas of individual epidermal cells, but similar in size to the mesh formed by the network of minor veins visible just beneath the skin. Susceptibility to orange peel differed among cultivars. Least susceptible were ‘Dönissens Gelbe’ and, ‘Gil Peck’, intermediate were ‘Sam’, ‘Kordia’, ‘Merchant’, and the sour cherry ‘Ungarische Traubige’, and most susceptible were ‘Adriana’, ‘Regina’, and ‘Hedelfinger’. Incidence of orange peel during storage was negatively related to relative humidity (more at lower humidities) but also developed at 100% RH in the absence of transpiration. Submerging fruit in water for 2 d partly reversed orange peel. There was no significant difference in the permeance of the skins or in turgors of cells of the outer mesocarp between fruit without and with orange peel. There was a significant difference between the osmotic potential of the flesh (more negative) and that of the skin (less negative). During storage, the osmotic potentials of flesh and skin both decreased slightly, but the difference between them remained constant. The results show water loss from the skin is causal in orange peel disorder. The water loss from the skin occurs both by two routes: (1) transpiration to the atmosphere and also (2) by osmotic dehydration to the flesh.
AB - Skin shrivelling of sweet cherry (Prunus avium L.), referred to here as ‘orange-peel’ disorder, compromises fruit appearance and thus market value. The objectives were to establish a protocol to describe and quantify orange peel disorder and to identify the mechanism and factors determining its incidence. Fruit was stored for 28 to 33 d at 2 °C and 76% RH and orange peel disorder was quantified as a topographical roughness using an interferometer or by rating the fruit for orange peel using a four-step scoring scheme. Fruit with orange peel disorder had a skin topography similar to that of a citrus fruit − just on a finer scale. Under the conditions of the test, orange peel was first visible after ∼7 d and continued to increase in severity thereafter. Orange peel was most severe on the shoulder and in the equatorial and distal regions of the fruit. There was no relationship between the distribution of orange peel and that of stomata or of microcracking. At a microscopic level, the depressions in the fruit surface were markedly larger than the periclinal areas of individual epidermal cells, but similar in size to the mesh formed by the network of minor veins visible just beneath the skin. Susceptibility to orange peel differed among cultivars. Least susceptible were ‘Dönissens Gelbe’ and, ‘Gil Peck’, intermediate were ‘Sam’, ‘Kordia’, ‘Merchant’, and the sour cherry ‘Ungarische Traubige’, and most susceptible were ‘Adriana’, ‘Regina’, and ‘Hedelfinger’. Incidence of orange peel during storage was negatively related to relative humidity (more at lower humidities) but also developed at 100% RH in the absence of transpiration. Submerging fruit in water for 2 d partly reversed orange peel. There was no significant difference in the permeance of the skins or in turgors of cells of the outer mesocarp between fruit without and with orange peel. There was a significant difference between the osmotic potential of the flesh (more negative) and that of the skin (less negative). During storage, the osmotic potentials of flesh and skin both decreased slightly, but the difference between them remained constant. The results show water loss from the skin is causal in orange peel disorder. The water loss from the skin occurs both by two routes: (1) transpiration to the atmosphere and also (2) by osmotic dehydration to the flesh.
KW - Cell wall
KW - Cuticle
KW - Permeance
KW - Shrivel
KW - Stomata
KW - Storage
KW - Transpiration
KW - Turgor
UR - http://www.scopus.com/inward/record.url?scp=85035754677&partnerID=8YFLogxK
U2 - 10.1016/j.postharvbio.2017.11.018
DO - 10.1016/j.postharvbio.2017.11.018
M3 - Article
AN - SCOPUS:85035754677
VL - 137
SP - 119
EP - 128
JO - Postharvest Biology and Technology
JF - Postharvest Biology and Technology
SN - 0925-5214
ER -