Pendrys J P
Mutat Res. 1983 Nov;122(2):129-33. doi: 10.1016/0165-7992(83)90049-0.
Recent measurements of the photorepair of UV-induced dimers in chick embryo fibroblasts have shown that the efficiency of photorepair is a function of time after UV exposure. Photorepair is enhanced if the time between UV exposure and photoreactivation is increased. A model is presented which fits the experimental data within the accuracy of the measurements. The disappearance of damaged sites follows first-order rate kinetics, similar to the kinetics of photorepair shown to exist in E. coli. However, some of the chromosomal DNA is protected from enzymatic activity, presumably by the histones and other proteins associated with eukaryotic DNA. The effective number of damaged sites available for repair increases monotonically with time after UV damage. At 37 degrees C all sites become available after 9-12 h. Immediately after UV exposure, about 75% of the DNA is shielded from photorepair.
近期对鸡胚成纤维细胞中紫外线诱导二聚体的光修复测量表明，光修复效率是紫外线照射后时间的函数。如果增加紫外线照射和光复活之间的时间间隔，光修复会增强。本文提出了一个模型，该模型在测量精度范围内符合实验数据。受损位点的消失遵循一级速率动力学，类似于在大肠杆菌中存在的光修复动力学。然而，一些染色体DNA受到保护，免受酶活性的影响，推测是通过与真核生物DNA相关的组蛋白和其他蛋白质。紫外线损伤后，可用于修复的有效受损位点数量随时间单调增加。在37摄氏度下，9至12小时后所有位点都变得可用。紫外线照射后立即有大约75%的DNA免受光修复。
