Goss P, Parsons P G
Int J Cancer. 1976 Mar 15;17(3):296-303. doi: 10.1002/ijc.2910170304.
Following exposure to ultraviolet irradiation (UV), two of three human fibroblast strains and one of three melanoma cell lines showed lower rates of thymine dimer excision during 24 h at 40 degrees C than at 36 degrees C. All lines had lower rates at 32 degrees C. Autoradiographic studies of three fibroblast strains and four melanoma lines incubated for four hours after irradiation revealed decreased unscheduled DNA synthesis at 42 degrees C compared with 36 degrees C. The rate of semiconservative DNA synthesis was decreased at the upper temperature in both series of experiments. All eight cell lines tested showed decreased repair at 42 degrees C, as judged by slower sedimentation and increased heterogeneity of parental DNA in alkaline sucrose gradients. Experiments using the DNA synthesis inhibitor Actinomycin D suggested that these effects were due to temperature-sensitive repair synthesis. In the two lines studied, preincubation of cells at 42 degrees C apparently increased the extent of UV damage. Although by no means conclusive, these results are consistent with the possibility that temperature-sensitive DNA repair is a contributory factor in some cases of solar carcinogenesis.
在暴露于紫外线照射(UV)后,三个人类成纤维细胞系中的两个以及三个黑色素瘤细胞系中的一个,在40℃下24小时内胸腺嘧啶二聚体切除率低于36℃时的切除率。所有细胞系在32℃时切除率均较低。对三个成纤维细胞系和四个黑色素瘤细胞系照射后孵育四小时的放射自显影研究显示,与36℃相比,42℃时非预定DNA合成减少。在这两个系列实验中,较高温度下半保留性DNA合成速率均降低。通过碱性蔗糖梯度中亲本DNA沉降较慢和异质性增加判断,所有测试的八个细胞系在42℃时修复均减少。使用DNA合成抑制剂放线菌素D的实验表明,这些效应是由于温度敏感的修复合成所致。在所研究的两个细胞系中,细胞在42℃下预孵育显然增加了紫外线损伤的程度。尽管这些结果远非结论性的,但与温度敏感的DNA修复在某些日光致癌病例中起作用的可能性是一致的。