Nolan W T, Thompson J E, Lepock J R, Kruuv J
Int J Radiat Biol Relat Stud Phys Chem Med. 1981 Feb;39(2):195-205. doi: 10.1080/09553008114550211.
The repair of sublethal radiation damage (SLD) in Chinese hamster (V79) cells was investigated as a function of temperature in the presence and absence of the membrane lipid perturbers, butylated hydroxytoluene (BHT) or adamantanone, which decrease the viscosity of the membrane lipids. Addition of 0.01 mM BHT to the cells significantly increased the amount of repair of SLD over controls from 0 to 25 degrees C but not from 30 to 37 degrees C. The amount of repair of SLD decreased as a function of temperature to about 20 degrees C and remained relatively constant thereafter till about 2.5 degrees C where it began to decrease again. The change in the amount of repair at approximately 20 degrees C coincides with a membrane lipid phase transition, as seen by spin labelling, in these cells. The repair of potentially lethal damage (PLD) was not increased by BHT at the two temperatures investigated (5 and 20 degrees C). In fact, additional PLD was expressed when cells were incubated post-irradiation at these temperatures. The results imply that at least a component of the SLD repair system is membrane associated and that the SLD and PLD repair systems are independent.
在中国仓鼠（V79）细胞中，研究了亚致死辐射损伤（SLD）的修复情况，该修复情况是温度的函数，研究过程中存在和不存在膜脂扰动剂丁基羟基甲苯（BHT）或金刚烷酮，这两种物质会降低膜脂的粘度。向细胞中添加0.01 mM BHT后，在0至25摄氏度范围内，与对照组相比，SLD的修复量显著增加，但在30至37摄氏度范围内则没有增加。SLD的修复量随温度降低至约20摄氏度，并在此后保持相对恒定，直至约2.5摄氏度时又开始下降。在大约20摄氏度时修复量的变化与这些细胞中通过自旋标记观察到的膜脂相变相吻合。在所研究的两个温度（5和20摄氏度）下，BHT均未增加潜在致死损伤（PLD）的修复。事实上，当细胞在这些温度下辐照后孵育时，会表现出额外的PLD。结果表明，SLD修复系统的至少一个组成部分与膜相关，并且SLD和PLD修复系统是独立的。
