- CHILLING INJURY IN TOMATO FRUIT 237
stored at 0◦C showed lower ACO activities than beans stored at 26◦C
(Etani and Yoshida 1987). Similarly, decreased ACO activity and subse-
quent low production of ethylene was reported in chilled bean leaves
and cucumber at 11◦Cand12◦C, respectively (Wang and Adams 1982).
However, addition of ACC to discs of cucumber leaves stored at 5◦C
resulted in increased ethylene production (Wang and Adams 1982),
indicating that ACC is the limiting factor in ethylene production at cool
storage (Hoffman and Yang 1980).
An inter-relationship between ethylene production and CI has been
proposed (Wang 1989). Cool storage promotes accumulation of ACS and
ACO mRNA (Watkins et al. 1990). A surge in ethylene production is
commonly observed in many chilling-sensitive species after removal
from cool storage to warmer temperatures (Woolf et al. 1997); that rise
in ethylene production is usually higher than typical basal or wound-
induced ethylene (Field 1981). This ethylene burst is a sign of cellu-
lar damage and was often correlated with the appearance of CI symp-
toms (Sfakiotakis and Dilley 1974; Wang and Adams 1980) as reported
in mango, pear, zucchini, orange, and grapefruit (Wang et al. 1985;
Schirra 1993; Lederman et al. 1997; Balandran-Quintana et al. 2003;
Lafuente et al. 2003). Lin et al. (1993), however, questioned the phys-
iological significance of enhanced ethylene production in CI develop-
ment. They argued that elevated ethylene production could be used to
indicate that chilling-sensitive tissues had been exposed to chilling tem-
perature but that this rise in ethylene production did not necessarily
signify its involvement in CI symptom development. Luengwilai and
Beckles (2010) suggested that the post-chilling burst in ethylene pro-
duction was not essential for initiation of CI in tomato fruit. In general,
it was proposed that the exposure of chilling-sensitive species to con-
ditions below or at the critical chilling temperature affected the activity
of membrane-bound enzymes, increasing their activation energy and
thus determining ethylene production (Field 1981). Since cell mem-
brane damage has long been considered the primary site of injury and
as ethylene receptors are predominantly localized in the endoplasmic
reticulum membrane (Chen et al. 2002), changes in cell membrane phys-
ical properties could affect ethylene perception (Rugkong et al. 2011).
However, it remains unclear whether chilling-induced ethylene pro-
motes the physiological and biochemical changes associated with chill-
ing damage or if it participates in the mechanism of adaptation to chill-
ing stress and/or subsequent defense against damage.
No consistent relationship was found between ethylene produc-
tion and CI severity among species (Watkins 2002). Most notably,
during low temperature storage ethylene production could either be