Ley R D, Sedita A, Grube D D, Fry R J
Cancer Res. 1977 Sep;37(9):3243-8.
The ultraviolet-light induction of DNA damage has been measured in the epidermis of hairless mice with the use of damage-specific endonucleases from Micrococcus luteus. The rates of induction of endonuclease-sensitive sites in HRS/J/Anl and Skh:hairless-1 mice were 6.1 +/- 0.5 X 10(-11) and 6.5 +/- 0.8 X 10(-11)/dalton/J/sq m from a FS40 fluorescent sun lamp (280 to 400 nm), respectively. Enzymatic photoreactivation with yeast photoreactivating enzyme showed that approximately 80% of the endonuclease-sensitive sites were cycloburyl pyrimidine dimers. In both strains of mice the pyrimidine dimers remained in high-molecular-weight DNA for 24 hr after irradiation. These data show that mouse epithelial cells in vivo have little or no capacity for the excision repair of pyrimidine dimers.
利用藤黄微球菌中损伤特异性核酸内切酶，对无毛小鼠表皮中DNA损伤的紫外线诱导情况进行了测定。来自FS40荧光太阳灯（280至400纳米）的辐射，在HRS/J/Anl和Skh:无毛-1小鼠中，核酸内切酶敏感位点的诱导率分别为6.1±0.5×10⁻¹¹和6.5±0.8×10⁻¹¹/道尔顿/焦耳/平方米。用酵母光复活酶进行酶促光复活表明，约80%的核酸内切酶敏感位点是环丁基嘧啶二聚体。在这两种品系的小鼠中，嘧啶二聚体在照射后24小时仍存在于高分子量DNA中。这些数据表明，体内的小鼠上皮细胞对嘧啶二聚体的切除修复能力很小或没有。
