At the early period of studying the effects of low temperature on chilling-sensitive plants (second half of XIX century), Saks' theory of plants death due to disorders in water regime was widely accepted. However, subsequent studies revealed narrowness of such interpretation of these data. Changes in water regime appeared to be the consequence rather than the main cause of the chilling injury [1]. In the middle of XX century, Zholkevich found that wilting of aerial organs resulted from the loss of water-retaining capacity, caused by alterations in the cytoplasm structure and a misbalance of metabolism, rather than from excessive transpiration at a slow water supply from roots [2].Based on observations of protoplasm viscosity at decreasing temperature, Belehradek (1935, cited after [1]) suggested that the viscosity plays a key role in chilling injury. The lower is the chill tolerance of a plant, the higher is the temperature at which "gelation" occurs, and the faster is the rise in the cytoplasm viscosity. A considerable increase in viscosity slows down biochemical reactions in the cytoplasm and disturbs metabolism, which leads to physiological disorders in nutrition, respiration, and growth. However, Zholkevich showed that the cytoplasm viscosity in cucumber plants decreased with the duration of chilling period, reaching the lowest value after 2.5-4 days. Thereafter, the viscosity gradually increased to the level characteristic of unchilled plants and could even exceed this level shortly before the plant death [2]. In severely damaged plants, the viscosity continued to increase after transferring the plants to warmth. According to the author's view [2], the increase in viscosity before the plant death represents the final degradation stage, unrelated to the first stage of injury; it aggravates injury, even after the transfer of plants to warmth.According to some papers published in the 1950-1960s, the more general cause of injury of chilling-sensitive plants subjected to prolonged chilling resides in metabolic disorders. The death of chilling-sensitive plants at chilling temperatures was supposedly related to the prevalence of degradation over synthesis. A disbalance between energy production by respiration and its effective consumption was thought to be a possible cause for changes in the cytoplasm structure and irreversible shifts in metabolism [1]. However, metabolic changes become apparent only at sufficiently long chilling periods and, similarly to changes in water regime, could not be the primary cause of chilling injury in most cases. It was shown that short intervals of chilling treatment do not drastically retard metabolism [3]. Accumulation of toxic metabolites due to disbalance in metabolism, which takes place during cooling of chilling-sensitive plants (toxic effect was considered one of the main causes of chilling injury [1, 2]), often occurs only after the transfer of chilled tissues to optimal conditions [4]; i.e., it is a result of secondary dysfunction, related to warming.Among the hypotheses on...