the same plant (tree) can be harvested year after year. In eight seasons (1974–75 to 1981–82),
the same 28 trees were randomly picked (north, south, east and west sides; upper and lower, in-
ner and outer fruit) at 14-day intervals for a total of more than 100 pickings. We know of no com-
parable testbed material for CI research.- A reporting method was developed whereby the results of each individual picking were reduced
to a single value, thus greatly facilitating statistical analysis of multiple experiments [116–118]. - The program both sought immediate commercial results for the Florida citrus industry and
provided training in basic research methods for a series of graduate students. Such training in-
volved rigid adherence to the classical scientific method (i.e., constant testing and evaluation
of hypotheses), evidence of which approach is singularly missing in many published reports
on CI.
The initial hypothesis was that CI involved a breakdown of the respiratory system, resulting in toxic
products of incomplete oxidation (typically acetaldehyde), which in turn caused the distinctive peel le-
sions. (Acetaldehyde was always detectable in the atmosphere around chilled fruit, and application of ex-
ogenous acetaldehyde caused superficially similar lesions). A report that hypobaric (vacuum) storage
greatly prolonged the useful lifetime of various products (at their usual recommended storage tempera-
tures) attributed this effect to the continual removal of endogenous ethylene [119]. So we tried hypobaric
storage of bananas at chilling temperatures. CI was completely controlled, which we attributed to contin-
ual removal of toxic acetaldehyde [120]. The same effect was soon confirmed for limes and mitochon-
drial respiration of CI-susceptible citrus fruits (limes and grapefruit) versus CI-resistant Florida-grown
Valencia oranges [121].
The hypothesis of the breakdown of the respiratory mechanism appeared to be true. (It still does, but
it is now regarded as a secondary effect). In “micro” respiratory studies with 5-mm peel disks, the banana
disks always chilled. In tissue culture, less than half the grapefruit peel disks chilled, which corresponded
well to the curious pattern of CI-induced peel lesions [122]. An unsolved mystery is why, in fruits such
as grapefruit and cucumber, the cells at the periphery of a necrotic lesion collapse and die while the im-
mediately adjacent cells surrounding the lesion remain healthy. Carbon dioxide (a standard respiratory
depressant) was found to minimize adenosine 5 -triphosphate (ATP) accumulation (apparent evidence for
CI-induced impairment of the ATP/ADP energy transfer system). There was no correlation with CI and
levels of three enzymes (pectinmethylesterase, polygalacturonase, and cellulase), which had been sus-
pected of involvement in lesion formation [123,124].
Because “controlled atmosphere storage” has long been commercially used for other products, the
effect of CO 2 in suppressing CI was investigated. Two treatments were tested: a prestorage treatment with
very high levels (e.g., 25%) of CO 2 and also storage atmospheres developed under differentially perme-
able plastic films [125–127]. Success in suppressing CI was sometimes notable, but with three discon-
certing caveats.
- The early-season sensitivity to CI, which traditionally had been considered to decrease with in-
creasing fruit maturity, was reappearing in late-season, very mature grapefruit. An alert gradu-
ate student, Kazuhide Kawada, found that such late-season susceptibility to CI had been reported
in some detail for California grapefruit as long as ago as 1936, but researchers had missed the
paper because it had been given an inappropriate title [128]. - Although extremely effective in early and midseason, CO 2 had absolutely no protective effect
on grapefruit picked after the new bloom (ca. mid-March). - The length of delay between picking and postharvest treatments sometimes had more protective
effect than the treatments being compared.
A new hypothesis was clearly called for, and the one produced was twofold: the tree and the fruit had
to be considered as a whole (fruit off tress in full “growth flush” obviously behaved very differently from
fruit from dormant trees), and the controlling mechanism between tree and fruit had to be growth regula-
tors (GRs). A working hypothesis that CI was promoted by gibberellins and prevented by abscissic acid
(ABA) was largely confirmed [129]. ABA, the protective “stress hormone,” apparently can be developed
either pre- or postharvest. Much of this material has been summarized elsewhere [130]. With this knowl-
edge, it is easy to understand the protective effect of various prestorage treatments, not only for grapefruit
28 GRIERSON