Five-day-old etiolated cucumber (Cucumis sativus L.) seedlings cv. Marketmore held at 2 degrees C for 72 h developed chilling injury, resulting in desiccation and collapse of the hypocotyl tissue and eventual plant death. Hypoxia-induced accumulation of ethanol and acetaldehyde led to tolerance of subsequent chilling, as evidenced by continued hypocotyl growth and freedom from injury. Attenuated accumulation of volatiles by applied bisulfite reduced 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 also induced by exposure of seedlings to volatile anesthetics including n-propanol, n-butanol, chloroform and halothane, suggesting that ethanol activity may result from fluidization of membrane lipids. This view is consistent with results which showed that ethanol activity was not associated with lipid metabolism. However, development of cold tolerance in ethanol-enriched tissues was time dependent, indicating that ethanol activity probably also entails biosynthetic event(s).
