Abstract

Green banana fruit manifested severe chilling injury after 5–7 days storage at 5°C and 80% relative humidity. (Severe chilling injury is described here as a failure of the fruit to ripen on removal to conditions conducive to normal ripening.) The recoverable “wall bound” peroxidase fraction exhibited a sharp decline during this initial period of stress. Subsequent storage of severely chilled fruit at. 5°C resulted in a gradual increase in the “soluble” peroxidase pool and a rise in “wall bound” peroxidase to levels comparable to normal green fruit. After 30 days storage of fruit at 5°C the “soluble” and “wall bound” fractions of peroxidase peaked and declined rapidly in the latter pool. The increase in peroxidase of cold stressed fruit involved qualitative changes in isozyme species that differed from those isozymes which emerge during normal fruit ripening. It is suggested that the initial decrease in “wall bound” peroxidase results in a loss in capability of the tissue to adapt to low temperature stress. The belated increase in peroxidase activity may be associated with a typical “cold hardening” response which develops only after an irreversible or “plastic strain” damage has occurred

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