Kadotani S, Arisawa M, Maruyama H B
Mutat Res. 1984 Nov-Dec;138(2-3):133-6. doi: 10.1016/0165-1218(84)90035-1.
The mutagenicity of 6 marketed non-steroidal anti-inflammatory drugs (aspirin, flufenamic acid, diclofenac sodium, indomethacin, naproxen and chloroquine) as well as 2 new anti-inflammatory drugs (tenoxicam and carprofen) was examined by using in vitro bacterial systems (repair test and reversion test). None of them was mutagenic on Ames' reversion test. However, they differed in their responses to repair tests. Tenoxicam, carprofen, aspirin, flufenamic acid and naproxen were not mutagenic in either rec- or pol-assays, whereas chloroquine only showed positive results in the pol-assay system. Indomethacin and diclofenac sodium exhibited a slightly stronger inhibitory activity against B. subtilis rec- mutant than against its rec+ counterpart in rec-assay, which was much weaker than AF-2. Thus their mutagenicity was questionable. These results confirm the usefulness of DNA-repair assays as a complementary endpoint to gene mutation in assessing the genotoxic potential of environmental compounds.
利用体外细菌系统(修复试验和回复突变试验)检测了6种市售非甾体抗炎药(阿司匹林、氟芬那酸、双氯芬酸钠、吲哚美辛、萘普生和氯喹)以及2种新型抗炎药(替诺昔康和卡洛芬)的致突变性。在艾姆斯回复突变试验中,它们均无致突变性。然而,它们对修复试验的反应有所不同。替诺昔康、卡洛芬、阿司匹林、氟芬那酸和萘普生在rec-或pol-试验中均无致突变性,而氯喹仅在pol-试验系统中显示阳性结果。在rec-试验中,吲哚美辛和双氯芬酸钠对枯草芽孢杆菌rec-突变体的抑制活性略强于对其rec+对应物的抑制活性,但其活性远弱于AF-2。因此,它们的致突变性存疑。这些结果证实了DNA修复试验作为评估环境化合物遗传毒性潜力的基因突变补充终点的有用性。