626 Produce Degradation: Reaction Pathways and their Prevention
Although the phase-change hypothesis has been disputed, the involvement of
the membrane in the response to chilling has been widely accepted. Lyons et al.^32
and Shewfelt^35 presented discussions of research that investigated membrane
responses to low temperature.
Whether the physical phase change of membranes leads to secondary responses
or irreversible changes is dependent on such factors as temperature, the length of
exposure, and the susceptibility of the plant species to a particular temperature.^33
Exposure of sensitive species to a chilling temperature may result in:
- loss of membrane integrity
- leakage of solutes
- loss of compartmentation
- decrease in the rate of mitochrondrial oxidative activity
- increase in the activation energy of membrane-associated enzymes
- cessation of protoplasmic streaming, reduction in energy supply and uti-
lization - decrease in photosynthetic rate
- disorganization of cellular and subcellular structure
- dysfunction and imbalance of metabolism, accumulation of toxic sub-
stances - manifestation of a variety of chilling injury symptoms
The effects of chilling may take time to develop, especially if the temperature
is not far below the critical temperature.^7 These effects may be reversible if the
chilling exposure is short but generally become irreversible with prolonged chilling.
Damage to cellular membranes as the primary effect of chilling injury was
reaffirmed by studies of ultrastructural changes associated with the development of
chilling injury. In tomatoes, plastid mitochondrial compartments degenerated several
days after chilling.^39 Some of the early chilling-related ultrastructural changes were
reversible with rewarming.
20.4.1.3.2 Stimulation of Ethylene Production
Although ethylene production is stimulated by chilling temperatures in a number of
plants, Wang and Adams^40 found that the pathway for ethylene biosynthesis in chilled
tissues was the same as that in ripening fruit. The step that was enhanced by the chilling
temperature was the synthesis of 1-aminocyclopropane-1-carboxylic acid (ACC), the
immediate precursor of ethylene. Increased ethylene production in chilled tissue was
the result of increased capacity of the tissue to make ACC. Generally, ACC levels, ACC
synthase activity, and ethylene production remained low while the tissue was held at
chilling temperatures. However, they increased when the tissue was removed to a
warmer temperature. Chilling-induced ethylene production declined after the initial
stimulation, even when endogenous ACC levels were still elevated.^40 These data suggest
that conversion of ACC to ethylene was the first step damaged by chilling.
Stimulation of ethylene production may not be a primary response to chilling.^40
Inhibition of chilling-induced ethylene production did not result in retardation of
chilling injury symptoms. Because ACC synthase, the key enzyme for ethylene