Heat treatment and fruit ripening

Postharvest heat treatments lead to an alteration of gene expression and fr uit ripening can sometimes be either delayed or disrupted. The extent of th e alternation of fruit ripening is a function of the exposure temperature a nd duration and how quickly the commodity is cooled following the heat trea tment. The most commonly measured components of fruit ripening affected by heat treatments include fruit softening, membrane and flavor changes, respi ration rate, ethylene production, and volatile production. Cell wall degrad ing enzymes and ethylene production are frequently the most disrupted and a re sometimes not produced or their appearance is delayed following heating. Other processes associated with ripening are not altered to the same exten t or soon recover. Fruit sensitivity to heat treatments is modified by preh arvest weather conditions, cultivar, rate of heating, and subsequent storag e conditions. The amount of sensitivity or tolerance to heat stress of a co mmodity is related to the level of heat protective proteins at harvest and the postharvest production of heat shock proteins. Two types of heat respon ses are seen. The first is a normal cellular response (< 42<degrees>C) that can lead to reduced chilling sensitivity, delayed or slowed ripening and a modification of quality. The second occurs near the threshold for damage > 45 degreesC and is modified by the pre-stress environmental conditions, th e cellular response to stress and cellular recovery. Loss of membrane integ rity appears to be an effect and not a cause of injury. The site of the inj ury lesion is still unknown and could be associated with transcription, tra nslation and cellular recovery capacity after an injury threshold has been exceeded. (C) 2000 Elsevier Science B.V. All rights reserved.