[The cellular reaction to heat shock: the physiological aspect]

This review regards the basic manifestations of cell response to heat-shock (HS): formation of resistance increase or acquired tolerance, and contribution of stress proteins (SP) to this reaction. This to great extent nonspecific increase in heat-shock cell resistance is based on two processes: a) an increase in the initial heat resistance of cell functions which results from enhancing of resistance of native efficient state of cell protein macromolecules to denaturating agents; b) stimulation of cell repair capacity that is expressed as an increase in the rate of cell function restoration in the case of its equal extent of damage in trained and untrained cells, and as expansion of the repairable zone (the interval of temperatures within the limits of which the function is inhibited completely, but reversibly after certain duration of heating). Stimulation of cell repair capacity is due to a more rapid renativation or substitution of proteins modified by stress. Both the processes (a and b) provide the ability of trained cells to function under higher temperature, compared to untrained ones. This review shows that heating, as well as any other denaturating agent as an inadequate stimulant, can give rise to synthesis of new proteins and other metabolites or to enhance running synthesis of substances. The fact of protein synthesis stimulation does not provide grounds to attribute an adaptive function to these proteins. SP are unable to increase the initial heat-resistance of cell functions, but participation of some SP (chaperons) in stimulation of cell repair capacity is highly probable. In the same time the repair of heat injured cells can take place without protein synthesis. In some cases the acquired tolerance remains for several weeks after HS. A comparison of cell responses to HS and to medium temperature increase within the tolerant limits (temperature adjustment) shows that their adaptive mechanisms are evidently different, although the increase in the initial heat resistance of some functions and stimulation of cell repair capacity take place under the temperature adjustment.