Effects of chronic exposure to ultraviolet B radiation on DNA repair in the dermis and epidermis of the hairless mouse
Effects of chronic exposure to ultraviolet B radiation on DNA repair in the dermis and epidermis of the hairless mouse
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DOI：
10.1046/j.1523-1747.2001.01192.x
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发表时间：
2001-02-01
影响因子：
6.5
通讯作者：
Lowery, MG
中科院分区：
文献类型：
--
作者：
Mitchell, DL;Byrom, M;Lowery, MG
此前已有研究表明，长期暴露于低剂量的紫外线B辐射会降低小鼠皮肤的DNA修复能力。在这项研究中，我们现在将其扩展到检查这一现象的浓度依赖性和组织依赖性。我们发现，(6-4)光产物的修复速度比环丁烷二聚体快得多，并且在真皮和表皮中光产物的去除动力学是相似的。慢性中波紫外线照射可显著降低DNA修复的初始速率和程度。低剂量的UVB(6-4)对光产物修复的影响最大，而大剂量的UVB(6-4)对环丁烷和(6-4)二聚体的修复作用减弱。而环丁烷二聚体修复在真皮中受到的影响最大，在两个组织中都观察到了减少的(6-4)光产物修复。在慢性治疗结束后，慢性紫外线照射的有害影响持续了相当长的一段时间。
It has previously been shown that chronic exposure to low fluences of ultraviolet B radiation reduced DNA repair capacity in mouse skin. In this study we now extend this to examine the concentration dependence and tissue dependence of this phenomenon. We found that (6-4) photoproducts were repaired considerably faster than cyclobutane dimers and that the kinetics for photoproduct removal were comparable in the dermis and epidermis. Chronic ultraviolet B irradiation significantly reduced the initial rate and extent of DNA repair. After low daily doses of ultraviolet B (6-4) photoproduct repair was most affected and after high daily doses the repair of both cyclobutane and (6-4) dimers was reduced. Whereas cyclobutane dimer repair was most affected in the dermis, reduced (6-4) photoproduct repair was observed in both tissues. The deleterious effects of chronic ultraviolet exposure were sustained for a considerable time after the chronic treatment ended.