Five-day-old etiolated cucumber (Cucumis sativus L. cv. Marketmore) seedlings held at 2C for 72 hours develop chilling injury resulting in desiccation and collapse of the hypocotyl tissues and eventual plant death. Hypoxia-induced accumulation of ethanol and acetaldehyde led to tolerance to subsequent chilling as evidenced by continued hypocotyl growth and freedom from injury. Arrest of volatile accumulation by applied bisulfite negated the development of hypoxia-induced chilling tolerance in seedlings. In seedlings held in normoxia, cold tolerance was induced by applied ethanol vapors, whereas acetaldehyde had a marginal effect, suggesting that hypoxia-induced cold tolerance may arise from the accumulation and activity of ethanol. Cold tolerance was induced by exposure to gaseous n-propanol and n-butanol vapors and other volatile anesthetics, including chloroform and halothane, indicating that ethanol activity may stem in part from an anesthetic effect that causes disorder of membrane lipids. However, development of cold tolerance in ethanol-enriched tissues was time-dependent, suggesting an association with biosynthetic event(s). Ethanol did not change the fatty acid composition in cucumber hypocotyl membranes.
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