Abstract

From the premise that desiccation‐induced damage is associated with a free‐radical mechanism of injury, we address the hypothesis that expression of desiccation damage is dependent on metabolism. The effects of temperature and O2 concentration on the expression of damage were studied in germinating bean (Phaseolus vulgaris L. cv. Pole Kentucky Wonder) axes and maize (Zea mays L. cv. Kelvedon Glory) radicles submitted to flash drying. Damage in desiccation‐tolerant and ‐intolerant material was assessed by measurements of electrolyte leakage and accumulation of a stable free radical. In desiccation‐tolerant material leakage rates remained low during water removal. In contrast, in desiccation‐intolerant tissues, leakage profiles revealed the presence of a critical moisture content below which leakage rates increased sharply. In the desiccation‐intolerant stage, a highly significant correlation was found between critical moisture contents and temperatures of drying. The concentration of the stable radical was lower if tissues were dried below 15°C and higher when tissues were dried at 30°C and above. Both leakage and build up of free radicals were highly sensitive to O2 concentrations: damage was lower when tissues were dried in the presence of N2, but increased several‐fold when tissues were exposed to O2 concentrations between 2 and 100%. In contrast, neither temperature nor O2 concentrations affected electrolyte leakage in desiccation‐tolerant samples. Treatment with a respiration inhibitor (KCN) prior to drying reduced the desiccation sensitivity of tissues, as noted by a reduction of the critical moisture content. We conclude that the expression of desiccation damage depends on the drying history and that factors that limit metabolism also reduce the incidence of desiccation injury.

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