Temperature Effects on Produce Degradation 625biochemical responses in plant tissue. Reviews such as those by Lyons et al.,^32
Wang,^33 Parkin et al.,^34 and Shewfelt^35 have looked at these responses as a means
of identifying possible mechanisms for chilling injury.
Researchers agree that control of chilling injury will not be possible until the
mechanism of this injury is fully understood. It also is agreed that, in order to fully
define the injury and its causes, a hypothesis for the mechanism of chilling injury
must meet several requirements.^34 It must account for the chilling response of all
sensitive plant tissues and for the progressively irreversible nature of injury during
prolonged periods of chilling stress. It must be consistent with the observation that,
in some chill-sensitive plants, chilling injury becomes evident only after the material
is transferred from the chilling environment to a warmer one. It must account for
the ability of some plants to acclimatize to adverse temperatures and for the varying
degrees of susceptibility to chilling injury of members within a genotype. Finally,
it must account for the fact that some plant materials are resistant to chilling injury.
Determination of the mechanism of chilling injury may be even further compli-
cated since, even within a single species, more than one mechanism may be involved.
For example, tomatoes are most susceptible to chilling injury at the mature green
and pink stages.^36 This would suggest that two distinct mechanisms may be involved
in the development of these conditions.
20.4.1.3.1 Changes in Cell Membranes
One of the first hypotheses to explain the nature of chilling injury was developed
by Lyons and Raison.^37 They proposed that chilling injury was the result of a physical
phase transition of membranes from a flexible liquid-crystalline to a solid-gel struc-
ture. This theory was based primarily on observations of Arrhenius breaks between
9 and 12°C for respiratory activity in mitochondria isolated from chilling-sensitive
tissue (tomato, cucumber, and sweet potato). These breaks were not evident in tissue
from chilling-resistant tissues (cauliflower, potato, and beets).
In subsequent work, Raison et al.^38 demonstrated that the activities of membrane-
associated enzyme systems were directly correlated to the physical state of the
membrane components. Chilling-resistant plants did not show the physical phase
transition of membranes or the sudden change in enzyme activity at chilling tem-
peratures.aSymptoms often become apparent only after removal to warm temperatures, as in marketing
bChilling sensitivity may be influenced by factors such as maturity at harvest, degree of ripeness, cultural
practices, and handling practices.
Source:Wang, C.Y., Chilling and freezing injury, in The Commercial Storage of Fruits, Vegetables, and
Florist and Nursery Crops, Gross, K. C., Yang, C. Y., and Saltveit, M., Eds., Agricultural Research Service,
Beltsville, MD, 2002, draft version of revised USDA Agriculture Handbook 66, available at
http://www.ba.ars.usda.gov/hb66/index.html. (With permission.)
TABLE 20.5
Fresh Produce Susceptibility to Chilling Injury When Stored at Low
but Nonfreezing Temperatures (continued)