Knowles R L, Eisenstark A
Division of Biological Sciences, University of Missouri, Columbia, MO 65211 USA.
Environ Health Perspect. 1994 Jan;102(1):88-94. doi: 10.1289/ehp.9410288.
We compared mutagenic spectra induced by polychromatic near-ultraviolet radiation (near-UV; 300-400 nm) with superoxide anion (O2-) -dependent mutagenesis using a set of Escherichia coli tester strains. Near-UV radiation produced increased frequencies of G:C to A:T transitions, G:C to T:A and A:T to T:A transversions, and small increases in frameshift mutations in wild-type cells. Tester strains lacking superoxide dismutase (SOD) activity (sodAsodB double mutants) demonstrated high spontaneous mutation frequencies and increased near-UV sensitivity. The double mutants also showed increased mutations induced by near-UV compared to either isogenic wild type, sodA or sodB single mutants. Furthermore, these mutants had an unusual spontaneous mutation spectrum, with a predominance of A:T to T:A transversions, followed by G:C to T:A transversions and frameshifts generated in runs of adenines in both the +1 and -1 direction. Other frameshifts were detected to a lesser degree. The oxygen dependency and the type of mutations spontaneously induced in SOD-deficient cells indicated that this mutagenic spectrum was caused by oxidative DNA damage. However, no apparent synergistic action between near-UV radiation and an increased flux of O2- could be detected. From the frequency and types of mutations induced by the two agents, we speculate that near-UV-induced mutagenesis and O2--dependent mutagenesis involve, in part, different lesion(s) and/or mechanism(s). The nature and possible mutagenic pathways of each are discussed.
我们使用一组大肠杆菌测试菌株,比较了多色近紫外辐射(近紫外;300 - 400 nm)诱导的诱变谱与超氧阴离子(O2-)依赖性诱变。近紫外辐射使野生型细胞中G:C到A:T的转换、G:C到T:A以及A:T到T:A的颠换频率增加,移码突变也有小幅增加。缺乏超氧化物歧化酶(SOD)活性的测试菌株(sodAsodB双突变体)表现出高自发突变频率和更高的近紫外敏感性。与同基因野生型、sodA或sodB单突变体相比,双突变体在近紫外诱导下也表现出更多的突变。此外,这些突变体具有不寻常的自发突变谱,以A:T到T:A的颠换为主,其次是G:C到T:A的颠换以及在腺嘌呤串中向+1和-1方向产生的移码突变。其他移码突变的检测程度较低。SOD缺陷细胞中自发诱导的突变的氧依赖性和类型表明,这种诱变谱是由氧化性DNA损伤引起的。然而,未检测到近紫外辐射与增加的O2-通量之间有明显的协同作用。从这两种因素诱导的突变频率和类型来看,我们推测近紫外诱导的诱变和O2-依赖性诱变部分涉及不同的损伤和/或机制。本文讨论了每种因素的性质和可能的诱变途径。