DNA复制抑制剂对同步化人类细胞紫外线切除修复的影响。
Effects of DNA replication inhibitors on UV excision repair in synchronised human cells.
作者信息
Downes C S, Collins A R
出版信息
Nucleic Acids Res. 1982 Sep 11;10(17):5357-68. doi: 10.1093/nar/10.17.5357.
Abstract
When HeLa cells are irradiated with UV and treated with the DNA synthesis inhibitors hydroxyurea (HU) and 1-beta-D-arabinofuranosylcytosine (ara C), DNA strand breaks accumulate at sites where excision repair of DNA damage has been inhibited after the incision step. This break accumulation occurs in mitotic, G1 and S phase cells. But UV-induced repair synthesis of DNA, as measured by [3H]thymidine incorporation into unreplicated DNA, is not inhibited by HU and ara C in G1 or S phase cells, even though replicative synthesis is virtually abolished. Repair and replication must therefore utilise different DNA precursor pools, or different DNA synthetic systems; and the action of Hu and ara C in causing strand break accumulation may occur at the ligation step of excision repair.
摘要
当用紫外线照射海拉细胞并用DNA合成抑制剂羟基脲（HU）和1-β-D-阿拉伯呋喃糖基胞嘧啶（ara C）处理时，DNA链断裂会在切口步骤后DNA损伤切除修复受到抑制的位点积累。这种断裂积累发生在有丝分裂期、G1期和S期细胞中。但是，通过将[3H]胸苷掺入未复制DNA来测量的紫外线诱导的DNA修复合成，在G1期或S期细胞中不受HU和ara C的抑制，尽管复制性合成实际上已被消除。因此，修复和复制必须利用不同的DNA前体池或不同的DNA合成系统；并且HU和ara C导致链断裂积累的作用可能发生在切除修复的连接步骤。
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本文引用的文献
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