Su Z Z, Cornelis J J, Rommelaere J
Carcinogenesis. 1981;2(10):1039-43. doi: 10.1093/carcin/2.10.1039.
The exposure of human or rat cells to non-toxic concentrations of two 2-nitronaphthofuran derivatives activated co-ordinately the transient expression of mutator and repair activities. These activities gave rise to both an increase in the mutagenesis (enhanced mutagenesis, EM) and survival (enhanced reactivation, ER) of unirradiated and u.v.-irradiated parvovirus H-1 used as respective probes. The kinetics of expression was the same for mutator and repair activities and for the two chemicals studied. The dose-responses of these activities were also parallel for a given chemical, but one of the furan derivatives exerted its inducing effect at concentrations 20-25 times lower than the other derivative. Both EM and ER were depressed by cycloheximide, and inhibitor of de novo protein synthesis. This is the first report which shows that chemicals can enhance the mutagenesis of undamaged DNA by activating the expression of mutator functions in mammalian, including human, cells. The ability of the two 2-nitronaphthofuran derivatives to trigger EM and ER was found to correlate with their reported mutagenicity in a conventional bacterial test system.
将人或大鼠细胞暴露于两种2-硝基萘并呋喃衍生物的无毒浓度下，可协同激活诱变和修复活性的瞬时表达。这些活性导致分别用作探针的未辐照和紫外线辐照的细小病毒H-1的诱变作用增加（增强诱变，EM）和存活率提高（增强复活，ER）。诱变和修复活性以及所研究的两种化学物质的表达动力学是相同的。对于给定的化学物质，这些活性的剂量反应也是平行的，但其中一种呋喃衍生物的诱导作用浓度比另一种衍生物低20-25倍。EM和ER均被环己酰亚胺（一种从头蛋白质合成抑制剂）抑制。这是第一份表明化学物质可通过激活哺乳动物（包括人类）细胞中诱变功能的表达来增强未受损DNA诱变作用的报告。发现这两种2-硝基萘并呋喃衍生物引发EM和ER的能力与其在传统细菌测试系统中报告的诱变性相关。
