Háva P, Hejlová A, Sosková L
Folia Microbiol (Praha). 1978;23(1):45-54. doi: 10.1007/BF02876595.
The effect of caffeine on nitrosoguanidine-induced mutagenesis of Salmonella typhimurium and its P22 and L phages was studied. The detected mutations included phage "clear" mutations, reversions of phage "amber" mutation, and prototrophic reversions of the his- auxotroph of Salmonella typhimurium. Neither the recA mutation of the host nor the erf mutation of the phage genome were found to affect the nitrosoguanidine-induced mutagenesis of the phage during vegetative growth. Beginning with a concentration of 0.2 mg/ml, caffeine decreased the frequency of mutants by 30--60%, attaining a maximum effect at 1.5 mg/ml and retaining this effect even at higher concentrations. A similar antimutagenic effect was observed with the mutagenesis of the host cells. The nitrosoguanidine-induced mutagenesis does not seem to be related to the function of the recA cell gene or the erf phage gene. The mechanism of mutagenesis by nitrosoguanidine probably has two components, one of them caffeine sensitive, the other caffeine-resistant.
研究了咖啡因对亚硝基胍诱导的鼠伤寒沙门氏菌及其P22和L噬菌体诱变的影响。检测到的突变包括噬菌体“清亮”突变、噬菌体“琥珀”突变的回复突变以及鼠伤寒沙门氏菌组氨酸营养缺陷型的原养型回复突变。未发现宿主的recA突变或噬菌体基因组的erf突变会影响营养生长期间亚硝基胍诱导的噬菌体诱变。从浓度0.2mg/ml开始,咖啡因使突变体频率降低30% - 60%,在1.5mg/ml时达到最大效果,甚至在更高浓度下仍保持这种效果。在宿主细胞诱变中也观察到类似的抗诱变作用。亚硝基胍诱导的诱变似乎与recA细胞基因或erf噬菌体基因的功能无关。亚硝基胍诱变的机制可能有两个组成部分,其中一个对咖啡因敏感,另一个对咖啡因耐药。