Jóźwiak Z, Leyko W
Chair of Biophysics, University of Lódź, Poland.
Int J Radiat Biol. 1992 Dec;62(6):743-56. doi: 10.1080/09553009214552701.
Exposure of cells to hyperthermia induces a transient resistance to subsequent heat treatment. The specific mechanisms responsible for hyperthermic cell killing and thermotolerance development are not well understood. It seems that heat may induce at least two different states of thermotolerance, of which one is dependent on protein synthesis. The expression of thermotolerance may include multiple cytoplasmic and membrane components. A number of studies have indicated that membranes play an important role in governing the thermal injury of cells. It seems, therefore, that heat denatured plasma membrane proteins may be a potential target for thermal stress and a trigger for the induction of thermotolerance. The localization of heat shock proteins in the plasma membrane and the suggestion of thermal resistance in enucleate erythrocytes support this suggestion. However, a direct relationship between the plasma membrane and hyperthermic killing or development of thermotolerance has not been found.
将细胞暴露于热疗会诱导其对后续热处理产生短暂抗性。导致热诱导细胞杀伤和热耐受性发展的具体机制尚未完全明确。似乎热可能诱导至少两种不同状态的热耐受性，其中一种依赖于蛋白质合成。热耐受性的表达可能包括多种细胞质和膜成分。许多研究表明，膜在控制细胞热损伤中起重要作用。因此，热变性的质膜蛋白可能是热应激的潜在靶点和诱导热耐受性的触发因素。热休克蛋白在质膜中的定位以及无核红细胞中热抗性的提示支持了这一观点。然而，尚未发现质膜与热诱导杀伤或热耐受性发展之间的直接关系。
