Sarasin A R, Hanawalt P C
Proc Natl Acad Sci U S A. 1978 Jan;75(1):346-50. doi: 10.1073/pnas.75.1.346.
Treatment of monkey kidney cells with low doses of carcinogen enhances the survival of UV-irradiated simian virus 40 (SV40). This is true for compounds with UV-like effects (metabolites of aflatoxin B1, N-acetoxyacetylaminofluorene) and compounds with x-ray-like effects (methyl methanesulfonate, ethyl methanesulfonate). This phenomenon resembles the UV-reactivation of viruses in eukaryotic cells. The carcinogen-induced enhancement of the survival of UV-irradiated SV40 is correlated with the inhibition of host-cell DNA synthesis, suggesting that the inhibition is an inducing agent. An enhancement of UV-irradiated SV40 survival is also obtained in cells treated with hydroxyurea or cycloheximide for long enough that there is still inhibition of host DNA synthesis during the early stage of SV40 infection. We hypothesize that treatment of host cells with carcinogens induces a new recovery pathway that facilitates the replication of damaged DNA, bypassing the lesions and resulting in the enhanced survival of UV-irradiated SV40. This inducible process might represent the expression of "SOS repair" functions in eukaryotic cells analogous to the previously demonstrated induction of SOS repair in bacteria after UV or carcinogen treatment.
用低剂量致癌物处理猴肾细胞可提高紫外线照射的猴病毒40（SV40）的存活率。对于具有紫外线样效应的化合物（黄曲霉毒素B1的代谢产物、N - 乙酰氧基乙酰氨基芴）和具有X射线样效应的化合物（甲基磺酸甲酯、乙基磺酸甲酯）来说都是如此。这种现象类似于真核细胞中病毒的紫外线复活。致癌物诱导的紫外线照射后SV40存活率的提高与宿主细胞DNA合成的抑制相关，这表明这种抑制是一种诱导剂。在用羟基脲或环己酰亚胺处理足够长时间的细胞中也能获得紫外线照射后SV40存活率的提高，以至于在SV40感染的早期阶段宿主DNA合成仍受到抑制。我们假设用致癌物处理宿主细胞会诱导一种新的修复途径，该途径有助于受损DNA的复制，绕过损伤部位，从而提高紫外线照射后SV40的存活率。这种可诱导过程可能代表真核细胞中“SOS修复”功能的表达，类似于之前在紫外线或致癌物处理后细菌中证明的SOS修复诱导。
