| In this study, 'Jin Kui' kiwifruit (Actinidia deliciosa) was employed in a series of studies to better understand fruit ripening and softening mechanisms. Effects of different biochemical substances on kiwifruit post-harvest physiological activities and the storage life were investigated. The results were as follows:1. Kiwifruit is a typical respiratory climactic fruit, and obvious respiration climacteric and ethylene release peak was observed 10-11 days after being harvested when fruits were kept at room temperature and at 20 ℃. While at 0℃, much less (20 times lower the peak) ethylene content was detected. It was observed that the fruit ripening process was divide into two obvious periods during storage (at room temperature, 20°C and 0℃) taking fruit firmness drop into account at first. And the fruit firmness dropped by two stages, i.e. the beginning sharply losing and the later slowly losing stages. At 0℃ fruit firmness drop was effectively delayed at the rapid losing of stage.2. Rapid decomposition of starch with increasing of amylase activity is the chief reason of fruit softening at the first stage, fruit firmness losing is positively correlated with starch degradation (r=0.99); and amylase was the key stage specific enzymes (SSE) for softening at this phase. At second stage the softening was caused by the degradation of insoluble pectin with increasing of polygalacturonase (PG) activity, therefore PG was the key SSE during the second softening stage. Also storage at 0℃ inhibited amylase and PG activity. The PME activity peak was appeared at 8 days and 21 days after harvest respectively at 20 ℃ and 0℃. SOD, CAT and POD all are inducible protect-enzymes, their activity peak were found at the later softening stage, storage at 0℃ kept their activity on a stable level so that the fruits might detect the damage of active oxygen and delay fruit senescence.3. Continuous decrease of endogenous ABA level from harvest was observed in kiwifruit fruits, though little wave of ABA content happened later, it suggested that the accumulation of ABA in fruit had terminated before harvest. The exogenous ABA treatment markedly enhanced the endogenous ABA level. The endogenous IAA and GA3 content of fruit increased at first after harvest then declined gradually to the lowest level.4. Exogenous ethephon and ABA treatments enhanced fruit respiration and ethylene production, consequently stimulating the loss of fruit firmness, speeding ripening and senescence process. Exogenous IAA and GA3 treatments inhibited kiwifruit ripening process, showing lessloss of fruit firmness, decreased ethylene production, and enhanced endogenous IAA level at the first stage, and maintaining higher GA3 content at second stage. The most effective tests were treatments with 50mg/kg IAA and 50mg/kg GA3, and higher concentrations IAA and GA3 treatment (100mg/kg) in contrast promoted fruit ripening.5. Salicylic acid showed the inhibition of fruit respiration and ethylene releasing rate at the first storage stage, but better result was obtained with Chitosan when the whole storage period was considered. Both treatments slowed not only the fruit metabolic activity, but also the cell membrane oxidation, and the most effective test was that with 2%(v/v) Chitosan.6. Fruit weight loss was slowed down by both Chitosan and Salicylic acid treatments, and the control effect of weight loss was positively related to the concentration applied. Salicylic acid inhibited Amylase activity, delaying the first softening stage; while PG activity was greatly lowered by Chitosan postponing the second softening stage. Chitosan had better softening inhibition than Salicylic acid at the whole storage period.7. The fruits treated by CaCl2 had less firmness loss, and such effect became more evident as the CaCl2 concentrations increased and was observed at the second softening stage, at which the pectin decomposition was the main softening cause. CaCl2 slowed down the ripening process through inhibiting PME and PG activity and so the insoluble pectin degradation rate. I... |
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