摘要
The relation between oxidative damage and viability loss of excised embryonic axes of Antiaris toxicaria subjected to rapid drying with silica gel at 15℃ was studied. Changes of survival rate, accumulation of thiobarbituric acid-reactive substances （TBARs）, activities of superoxide dismutase （SOD）, catalase （CAT）, ascorbate peroxidase （APX）, glutathione reductase （GR） and the permeability of cell membrane that was determined as relative electrolyte leakage （REL） were measured. The half-life moisture content （MC,50） was 0.41 g H=O/g DW （dry weight basis）. During drying, the activities of SOD, CAT and APX increased until MCL50, and declined thereafter. The generation speed of ·O2-, and content of H2O2 and TBARs remained steadily or even decreased at MC levels higher than MC,s0, demonstrating a low oxidative level in these axes. There was no significant correlation between viability loss and accumulation of reactive oxygen species or lipid peroxidation within the dehydration process until MCLs0. Whereas the increase in REL from the beginning of the drying process indicated that the cell membrane was damaged. In conclusion, under rapid drying with silica gel the viability loss of excised recalcitrant A. toxicaria axes seemed to be triggered by mechanical or physical damage, rather than metabolic damage.
The relation between oxidative damage and viability loss of excised embryonic axes of Antiaris toxicaria subjected to rapid drying with silica gel at 15℃ was studied. Changes of survival rate, accumulation of thiobarbituric acid-reactive substances （TBARs）, activities of superoxide dismutase （SOD）, catalase （CAT）, ascorbate peroxidase （APX）, glutathione reductase （GR） and the permeability of cell membrane that was determined as relative electrolyte leakage （REL） were measured. The half-life moisture content （MC,50） was 0.41 g H=O/g DW （dry weight basis）. During drying, the activities of SOD, CAT and APX increased until MCL50, and declined thereafter. The generation speed of ·O2-, and content of H2O2 and TBARs remained steadily or even decreased at MC levels higher than MC,s0, demonstrating a low oxidative level in these axes. There was no significant correlation between viability loss and accumulation of reactive oxygen species or lipid peroxidation within the dehydration process until MCLs0. Whereas the increase in REL from the beginning of the drying process indicated that the cell membrane was damaged. In conclusion, under rapid drying with silica gel the viability loss of excised recalcitrant A. toxicaria axes seemed to be triggered by mechanical or physical damage, rather than metabolic damage.
