Arnold W R, Rainbow A J
Department of Biology, McMaster University, Hamilton, Ontario, Canada.
Mutagenesis. 1996 Jan;11(1):89-94. doi: 10.1093/mutage/11.1.89.
In this study we have utilized the ability of rodent cells to replicate viral DNA following semi-permissive infection by human adenovirus (Ad) to examine the host cell reactivation (HCR) of radiation-damaged Ad in several UV-sensitive Chinese hamster ovary (CHO) cell mutants. A significant reduction in HCR of viral DNA synthesis for UV-irradiated Ad was detected in a series of UV-sensitive mutants from complementation groups 1-6 derived from parental CHO-AA8 cells. HCR for UV-irradiated Ad in these CHO mutants varied from 18.8 to 48.0% of that in parental AA8 cells. However, a significant reduction in HCR of viral DNA synthesis for UV-irradiated Ad could not be detected in series of UV-sensitive PV mutants from complementation groups 1, 5, 9 and 10 derived from parental CHO-K1 cells, which harbour relatively small DNA repair deficiencies. We also report a reduced HCR for gamma-irradiated Ad in UV-sensitive CHO cell mutants from groups 1 and 4 derived from parental CHO-AA8 cells. This HCR technique for DNA synthesis of Ad can be employed to measure the DNA repair capacity of both human and rodent cells and extended to examine the repair of DNA damaged by a variety of different physical and chemical agents.
在本研究中，我们利用啮齿动物细胞在受到人腺病毒（Ad）半允许感染后复制病毒DNA的能力，来检测几种对紫外线敏感的中国仓鼠卵巢（CHO）细胞突变体中受辐射损伤的Ad的宿主细胞复活（HCR）情况。在一系列源自亲本CHO-AA8细胞的1-6互补组的紫外线敏感突变体中，检测到紫外线照射的Ad的病毒DNA合成的HCR显著降低。这些CHO突变体中紫外线照射的Ad的HCR为亲本AA8细胞的18.8%至48.0%。然而，在一系列源自亲本CHO-K1细胞的1、5、9和10互补组的紫外线敏感PV突变体中，未检测到紫外线照射的Ad的病毒DNA合成的HCR显著降低，这些突变体的DNA修复缺陷相对较小。我们还报告了源自亲本CHO-AA8细胞的1和4组紫外线敏感CHO细胞突变体中γ射线照射的Ad的HCR降低。这种用于Ad DNA合成的HCR技术可用于测量人和啮齿动物细胞的DNA修复能力，并扩展到检测由各种不同物理和化学剂损伤的DNA的修复情况。
