Chilling at 4°C in the dark induced lipid degradation in cucumber (Cucumis sativa L.) fruit upon rewarming at 14°C. Rates of ethane evolution by fruits rewarmed after 3 days of chilling were up to four-fold higher than those evolved by unchilled (140C) fruits (0.02-0.05 picomoles gram fresh weight-1 hour-'). This potentiation of lipid peroxidation occurred prior to irreversible injury (requiring 3 to 7 days of chilling) as indicated by increases in ethylene evolution and visual observations. Decreases in unsaturation of peel tissue glycolipids were observed in fruits rewarmed after 3 days of chilling, indicating the plastids to be the site of the early phases of chilling-induced peroxidation. Losses in unsaturation of tissue phospholipids were first observed only after chilling for 7 days. Phospholipase D activity appeared to be potentiated in fruits rewarmed after 7 days of chilling as indicated by a decrease in phosphatidylcholine (and secondarily phosphatidylethanolamine) with a corresponding increase in phosphatidic acid. These results indicate that lipid peroxidation may have a role in conferring chilling injury.examined as a primary response to chilling stress (in the absence of illumination), there is indirect evidence in the literature that suggests it may have a role in the development of chilling injury. The application of antioxidants to cucumber and pepper fruits delayed or reduced the severity of low temperature injury (26). Chilling also evokes a decrease in catalase activity in cucumber seedlings (18). These studies indicate that antioxidant defenses may be compromised in some CS plants exposed to low temperatures. In the special case where chilling is accompanied by illumination, photooxidation of cellular membranes is believed to play a role in the development of CI (22,28,29).We propose that lipid peroxidation may have a role in the development of CI, and undertook a study to provide an initial evaluation of this new hypothesis. Cucumber fruits were used as a model since the visual manifestations ofchilling injury in this tissue are well-defined (25, 26). There is also a lack of studies on CI in fruit tissues compared to whole plants, leaves, and other organs. Fruits were chilled in the absence of light to eliminate the contribution ofphotooxidative processes in the development of injury.Several theories have been advanced to account for the nature of CO.2 The primary lesion has been proposed to involve bulk membrane lipid phase transitions (12), unfavorable and direct low temperature effects on proteins and enzymes (7), the presence of high-melting membrane lipid species (15), and a redistribution of cellular calcium (13). Although data are available to support each of these theories, none appears to be universally accepted as the primary determinant of CI. The existence of a universal mechanism of CI is questionable and alternatively, several of the aforementioned factors may be required to confer low temperature sensitivity. There is also the possibility that some other unidentified ...