Kampinga H H
Department of Radiobiology, Faculty of Medicine, University of Groningen, The Netherlands.
J Cell Sci. 1993 Jan;104 ( Pt 1):11-7. doi: 10.1242/jcs.104.1.11.
Cells that have been pre-exposed to thermal stress can acquire a transient resistance against the killing effect of a subsequent thermal stress. The cause for this phenomenon, called thermotolerance, seems to be an enhanced resistance of proteins against thermal denaturation and aggregation. This resistance can be expressed as an attenuation of damage formation (less initial damage) or as a better repair of the protein damage (facilitated recovery). Heat Shock (or better, Stress) Proteins (HSPs) may play a role in and even be required for thermal resistance. However, rather than stress-induced enhanced synthesis and elevated total levels of HSPs per se, the concentration of, both constitutive and inducible, HSPs at and/or (re)distributed to specific subcellular sites may be the most important factor for the acquisition of thermotolerance. Specific HSPs may be involved either in damage protection or in damage repair.
预先暴露于热应激的细胞能够获得对随后热应激杀伤作用的短暂抗性。这种被称为热耐受性的现象的原因，似乎是蛋白质对热变性和聚集的抗性增强。这种抗性可以表现为损伤形成的减弱（初始损伤较少）或蛋白质损伤的更好修复（促进恢复）。热休克（或者更确切地说，应激）蛋白（HSPs）可能在热抗性中发挥作用，甚至是热抗性所必需的。然而，获得热耐受性的最重要因素可能不是应激诱导的HSPs合成增强和总水平升高本身，而是组成型和诱导型HSPs在特定亚细胞位点的浓度以及/或者（重新）分布。特定的HSPs可能参与损伤保护或损伤修复。
