Kinsella A R
Carcinogenesis. 1981;2(1):43-7. doi: 10.1093/carcin/2.1.43.
12-O-Tetradecanoyl-phorbol-13-acetate (TPA) was tested for its effect on N'-methyl-N'-nitro-N-nitrosoguanidine (MNNG) induced forward mutagenesis to 6-thioguanine resistance (6TGR) in V79 Chinese hamster cells. Using a replating assay, no effect of TPA on the recovery of 6TGR mutants was observed. Previous reports of TPA enhancement of carcinogen-induced forward mutagenesis using the in situ mutagenesis assay, can be explained in terms of the influence of metabolic co-operation on mutant recovery. TPA is known to eliminate metabolic co-operation, an artefact of the in situ mutagenesis assay system, thus contributing to the enhancement of mutant recovery in TPA treated cultures. This investigation aims to demonstrate that TPA has no influence on mutagenesis per se, positive or negative enhancement of forward mutagenesis being solely a reflection of the mutagenesis assay employed.
检测了12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)对N'-甲基 - N'-硝基 - N - 亚硝基胍(MNNG)诱导V79中国仓鼠细胞正向突变产生6 - 硫鸟嘌呤抗性(6TGR)的影响。采用再平板接种试验,未观察到TPA对6TGR突变体恢复的影响。先前关于使用原位诱变试验TPA增强致癌物诱导正向诱变的报道,可以从代谢协同作用对突变体恢复的影响方面进行解释。已知TPA可消除代谢协同作用,这是原位诱变试验系统的一种人为现象,从而有助于提高TPA处理培养物中突变体的恢复率。本研究旨在证明TPA本身对诱变没有影响,正向诱变的正向或负向增强仅仅反映了所采用的诱变试验。