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IntroductionAs all biologists appreciate, there is constant interaction between life and the environment, and temperature plays a critical role. It establishes distribution limits, it affects rates of function as well as the survival of organisms. Notoriously sensitive to temperature is plant growth. Critical steps in plant life such as germination, flowering and breaking of dormancy can be manipulated by the application of certain temperature treatments.Animal life is mainly limited to a narrow range of temperatures, from a few degrees below the freezing point of water to approximately 50 'C. Animals nevertheless differ in the range of temperatures that they can tolerate. Temperature tolerance may however change with time and a certain degree of adaptation is possible. The limits of temperature tolerance for a given animal are not fixed. Indeed, it has been known for some time that exposure to a near lethal temperature often leads to a degree of adaptation so that a previously lethal temperature is tolerated. This particular response to heat shock has attracted considerable attention from molecular biologists over the last decade, which has resulted in a rapid accumulation of data providing considerable insights, not only into the molecular basis of acquired thermotolerance, but into stress physiology in general. The heat shock response is now known to occur in bacteria and in plants as well as in animals, and is a rapid but transient reprogramming of cellular activities to ensure survival during the stress period, to protect essential cell components against heat damage and to permit a rapid resumption of normal cellular activities during the recovery period.

Chilling of Arabidopsis thaliana (L.) Heynh. callus tissue to 4 degrees C led to conditions of oxidative stress, as indicated by increased levels of the products of peroxidative damage to cell membranes. Cellular H2O2 was also observed to increase initially upon chilling but by day 8 cellular levels had declined to below control levels. Although levels of catalase activity remained similar to those in unchilled tissue, activity of ascorbate peroxidase increased between days 4 and 8 of chilling to 4 degrees C. In callus held at 23 degrees C, levels of reduced glutathione remained static whereas they rose in callus held at 4 degrees C. Levels of oxidised glutathione were initially low but increased significantly by day 4 in the chilled callus. At 23 degrees C, however, levels of oxidised glutathione remained low. Between days 1 and 3 at 4 degrees C, levels of glutathione reductase activity increased but by day 8 glutathione reductase activity was similar to that in cells held at 23 degrees C. Exposure of callus to abscisic acid at 23 degrees C also led to increased activities of ascorbate peroxidase and glutathione reductase.

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