Suzuki N, Nishimaki J, Kuwata T
Mutat Res. 1982 Dec;106(2):357-76. doi: 10.1016/0027-5107(82)90116-6.
Characterization was performed of a UV-resistant variant strain. UVr-10, derived from a human clonal cell line, RSb, with high sensitivity not only to the lethal effect of 254-nm far-ultraviolet (UV) irradiation but also to the effects of 4-nitroquinoline 1-oxide (4NQO) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and to the cell proliferation inhibition (CPI) effect of human leukocyte interferon (HuIFN-alpha) preparations. Colony-formation assays confirmed the increased resistance of UVr-10 cells to both UV and 4NQO, but no increased resistance to MNNG. The marked recovery from the inhibition of the total cellular DNA synthesis of UVr-10 cells, estimated by [methyl-3H]thymidine ([3H]dThd) uptake into the cellular DNA materials, was seen during 6 h after UV irradiation or 4NQO treatment even under the conditions without the recovery uptake into those of the parent RSb cells, but not during 6 h after MNNG treatment. Comparative studies on the activity of DNA repair synthesis between UVr-10 and RSb cells, by measuring the extent of UV-, 4NQO- or MNNG-induced unscheduled DNA synthesis (UDS) and DNA repair replication, revealed an increased activity of UVr-10 cells to UV and 4NQO but no significant increase of the activity to MNNG. These results suggest that increased DNA repair activities of a UVr-10 cell line may account for its becoming resistant to the lethal effect of UV and 4NQO. Concerning the CPI effect of HuIFN-alpha, UVr-10 cells showed increased resistance. Further, the DNA synthesis activity of UVr-10 cells was not so inhibited by HuIFN-alpha exposure as that of RSb cells. However, HuIFN-alpha-exposed UVr-10 cells showed more enhanced levels of activity of pppA(2'p5'A)n synthetase (2-5A synthetase) than the exposed RSb, thus suggesting that HuIFN-alpha could exert enough intracellular effect even in UVr-10 cells. The implication of the increased resistance of UVr-10 cells to the effects of UV, 4NQO and HuIFN-alpha, but not to those of MNNG, is discussed.
对一种抗紫外线变异株UVr - 10进行了特性鉴定。该变异株源自人克隆细胞系RSb，不仅对254纳米远紫外线（UV）照射的致死效应高度敏感，而且对4 - 硝基喹啉1 - 氧化物（4NQO）和N - 甲基 - N' - 硝基 - N - 亚硝基胍（MNNG）的效应以及人白细胞干扰素（HuIFN - α）制剂的细胞增殖抑制（CPI）效应也高度敏感。集落形成试验证实UVr - 10细胞对UV和4NQO的抗性增加，但对MNNG的抗性未增加。通过将[甲基 - 3H]胸苷（[3H]dThd）摄取到细胞DNA物质中来估计，UVr - 10细胞总细胞DNA合成抑制的显著恢复在UV照射或4NQO处理后的6小时内可见，即使在亲本RSb细胞没有恢复摄取的条件下也是如此，但在MNNG处理后的6小时内未观察到。通过测量UV、4NQO或MNNG诱导的非预定DNA合成（UDS）和DNA修复复制的程度，对UVr - 10和RSb细胞之间的DNA修复合成活性进行比较研究，结果显示UVr - 10细胞对UV和4NQO的活性增加，但对MNNG的活性没有显著增加。这些结果表明，UVr - 10细胞系DNA修复活性的增加可能是其对UV和4NQO致死效应产生抗性的原因。关于HuIFN - α的CPI效应，UVr - 10细胞表现出抗性增加。此外，UVr - 10细胞的DNA合成活性不像RSb细胞那样受到HuIFN - α暴露的强烈抑制。然而，与暴露的RSb细胞相比，暴露于HuIFN - α的UVr - 10细胞显示出更高水平的pppA(2'p5'A)n合成酶（2 - 5A合成酶）活性，因此表明HuIFN - α即使在UVr - 10细胞中也能发挥足够的细胞内效应。本文讨论了UVr - 10细胞对UV、4NQO和HuIFN - α的效应产生抗性增加而对MNNG的效应不产生抗性增加的意义。
