ALLEVIATION OF CHILLING INJURY, AND ITS MECHANISMS TO MARSH AND REDBLUSH GRAPEFRUIT (CITRUS PARADISI MACF.).

Abstract

The sensitivity of Arizona-grown grapefruit to chilling temperatures varied throughout the harvest period studied. This sensitivity was high in October, decreased in November and December, then increased in February. In April and May there was another decrease in sensitivity to chilling temperatures. Coating fruit with vegetable oils or fats successfully delayed the development of chilling injury and reduced the degree of injury, however, vegetable oils applied as water emulsions were even more effective in preventing chilling injury to 'Redblush' grapefruit extending the period of marketability more than 100 days. Postharvest application of CaCl₂ and certain plant growth regulators significantly increased the resistance of 'Marsh' grapefruit to chilling injury, but less so than oil emulsions. Scanning electron microscope photomicrographs of 'Marsh' grapefruit peels showed that severe chilling injury was a depressed area of collapsed cell, just beneath the epidermis layer. As the severity of chilling injury increased, non-collapsed cells gradually increased in size. Cell walls were irregularly shaped; thin in some areas and thick in others. Oil glands in depressed areas were not ruptured during cold storage. Hence release of toxic materials through rupturing of oil glands is not a factor in chilling injury. Compared to non-injured tissue, injured tissue from the same fruits had significantly lower water and osmotic potentials, and low, near zero, turgor pressures. There was a significant negative correlation (r = -0.5; p < 0.05) between the water potentials of the peels and the percentage of 'Marsh' grapefruit with severe chilling injury during storage at 2.8C. Ion leakage tended to increase during cold storage, and when the fruit were transferred to room temperature. Internal conductivities declined sharply during cold storage and then increased very strongly during periods at room temperature.