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照射后不久小鼠表皮中紫外线诱导的DNA损伤的去除。

Removal of UV-induced DNA lesions in mouse epidermis soon after irradiation.

作者信息

Vink A A, Henegouwen B, Nikaido O, Baan R A, Roza L

机构信息

TNO Medical Biological Laboratory, Rijswijk, Netherlands.

出版信息

J Photochem Photobiol B. 1994 Jun;24(1):25-31. doi: 10.1016/1011-1344(94)07005-9.

Abstract

Induction and removal of cyclobutane thymine dimers and (6-4)photoproducts were studied in epidermal DNA isolated from UV-exposed hairless mice. For the detection of DNA damage, lesion-specific monoclonal antibodies were used in an immunoslotblot assay. Following the exposure of mice to 3.0 kJ m-2 UV-B, substantial removal of both thymine dimers (66%) and (6-4)photoproducts (77%) was observed at 24 h after irradiation. No removal, however, was detected at 4 h after irradiation. In contrast, immunofluorescence data obtained previously showed a rapid initial dimer removal after irradiation with 1.0 kJ m-2 UV-B (A.A. Vink, R.J.W. Berg, F.R. De Gruijl, L. Roza and R.A. Baan, Carcinogenesis, 12 (1991) 861-864). Reinvestigation of the removal of dimers and (6-4)-photoproducts shortly after three different UV doses showed a rapid decreases of both lesions at 2 h after irradiation with 1.0 kJ m-2. The results obtained after irradiations with 2.0 and 3.0 kJ m-2 UV-B suggest a saturation of repair already at 2.0 kJ m-2. Cyclobutane dimers were found to be removed at a lower rate than (6-4)photoproducts.

摘要

在从紫外线照射的无毛小鼠分离的表皮DNA中,研究了环丁烷胸腺嘧啶二聚体和(6-4)光产物的诱导和去除情况。为了检测DNA损伤,在免疫斑点印迹分析中使用了损伤特异性单克隆抗体。将小鼠暴露于3.0 kJ m-2的UV-B后,在照射后24小时观察到胸腺嘧啶二聚体(66%)和(6-4)光产物(77%)均有大量去除。然而,在照射后4小时未检测到去除情况。相比之下,先前获得的免疫荧光数据显示,在用1.0 kJ m-2的UV-B照射后,二聚体最初有快速去除(A.A. Vink、R.J.W. Berg、F.R. De Gruijl、L. Roza和R.A. Baan,《癌变》,12(1991)861-864)。在三种不同紫外线剂量照射后不久,对二聚体和(6-4)光产物去除情况的重新研究表明,在用1.0 kJ m-2照射后2小时,两种损伤均迅速减少。用2.0和3.0 kJ m-2的UV-B照射后获得的结果表明,在2.0 kJ m-2时修复已达到饱和。发现环丁烷二聚体的去除速率低于(6-4)光产物。

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