Repair of pyrimidine(6-4)pyrimidone photoproducts in mouse skin.
Repair of pyrimidine(6-4)pyrimidone photoproducts in mouse skin.
复制标题
小鼠皮肤中嘧啶(6-4)嘧啶酮光产物的修复。
DOI：
10.1111/1523-1747.ep12873312
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Epstein,JH
中科院分区：
文献类型：
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作者：
Mitchell,DL;Cleaver,JE;Epstein,JH
用放射免疫分析法测定了紫外线照射无毛小鼠表皮DNA中环丁烷嘧啶二聚体和嘧啶（6-4）嘧啶酮光产物的诱导和修复。紫外线（UV）照射后48小时切除几个环丁烷二聚体，而50%的（6-4）光产物被删除6小时，与先前确定的小鼠皮肤中的非程序性DNA合成率。在（6-4）光产物切除的初始快速阶段之后，在6和48小时之间观察到较慢的阶段。这些修复动力学与来自用UV光照射的小鼠组织的成纤维细胞培养物的那些形成对比，产生类似水平的损伤。虽然在培养的成纤维细胞和表皮细胞中（6-4）光产物修复的初始速率相似，但在培养的细胞中修复的程度明显更大，大部分损伤在24小时内被消除。小鼠表皮细胞中（6-4）光产物修复的动力学表明，显著的群体，如终末分化的角质形成细胞，可能具有降低的修复能力，并且培养过程可能选择更快速增殖的、修复能力强的干细胞。
The induction and repair of cyclobutane pyrimidine dimers and pyrimidine(6–4)pyrimidone photoproducts in the epidermal DNA of ultraviolet-irradiated hairless mice were determined by radioimmunoassay. Few cyclobutane dimers were excised by 48 h after ultraviolet (UV) irradiation, whereas 50% of the (6–4) photoproducts were removed by 6 h, correlating with previously determined rates of unscheduled DNA synthesis in mouse skin. After this initial rapid phase of (6–4) photoproduct excision, a slower phase was observed between 6 and 48 h. These repair kinetics contrast with those for fibroblast cell cultures derived from mouse tissues irradiated with UV light yielding similar levels of damage. Although the initial rate of (6–4) photoproduct repair in cultured fibroblasts and epidermal cells was similar, the extent of repair in cultured cells was significantly greater, with most of the damage removed by 24 h. The kinetics for (6–4) photoproduct repair in mouse epidermal cells suggest that a significant population, such as terminally differentiated keratinocytes, may have a reduced repair capacity and that the culture process may select for more rapidly proliferating, repair-proficient stem cells.