Aleksandrov V Ia, Kisliuk I M
Tsitologiia. 1994;36(1):5-59.
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.
本综述探讨了细胞对热休克（HS）反应的基本表现：抗性增加或获得性耐受的形成，以及应激蛋白（SP）在该反应中的作用。这种在很大程度上非特异性的热休克细胞抗性增加基于两个过程：a）细胞功能初始耐热性的增加，这是由于细胞蛋白质大分子天然有效状态对变性剂的抗性增强所致；b）细胞修复能力的刺激，表现为在训练有素和未训练的细胞损伤程度相同的情况下，细胞功能恢复速率的增加，以及可修复区域的扩大（温度区间，在此区间内功能完全被抑制，但在一定加热时间后可逆）。细胞修复能力的刺激是由于应激修饰的蛋白质更快地复性或替代。与未训练的细胞相比，这两个过程（a和b）都赋予了训练有素的细胞在更高温度下发挥功能的能力。本综述表明，加热以及任何其他作为不适当刺激物的变性剂，都可导致新蛋白质和其他代谢产物的合成增加或物质合成的加速进行。蛋白质合成受刺激这一事实并不能成为将这些蛋白质赋予适应性功能的依据。SP无法增加细胞功能的初始耐热性，但一些SP（伴侣蛋白）很可能参与刺激细胞修复能力。同时，热损伤细胞的修复可以在没有蛋白质合成的情况下发生。在某些情况下，获得性耐受在热休克后可持续数周。对细胞对热休克和耐受范围内中等温度升高（温度调节）的反应进行比较表明，尽管在温度调节下某些功能的初始耐热性增加和细胞修复能力受到刺激，但它们的适应性机制明显不同。
