Callen D F, Mohn G R, Ong T M
Mutat Res. 1977 Oct;45(1):7-11. doi: 10.1016/0027-5107(77)90037-9.
The ability of aflatoxins B1 and G1 to induce back mutations to arg+ in Escherichia coli K-12/343/113 was compared with the induction of mitotic gene conversion to ade+ in the diploid yeast strain Saccharomyces cerevisiae D4, ade-2. In analogy to previous results with other microorganisms, the compounds were not genetically active per se, indicating that under the experimental conditions employed none of the tester strains were able to activate the compounds to mutagenic products. In experiments using liver homogenates (S-9 fraction) of male Golden Syrian hamsters previously treated with phenobarbital, aflatoxin B1 exhibited strong genetic activity both in E. coli and in S. cerevisiae, whereas the mutagenic activity of aflatoxin G1 was markedly lower and could be detected only in the E. coli tester strain. These results correlate the findings that aflatoxin G1 is a less potent carcinogen and mutagen than aflatoxin B1.
将黄曲霉毒素B1和G1诱导大肠杆菌K-12/343/113回复突变为arg+的能力,与在二倍体酵母菌株酿酒酵母D4、ade-2中诱导有丝分裂基因转换为ade+的能力进行了比较。与先前对其他微生物的研究结果类似,这些化合物本身没有遗传活性,这表明在所采用的实验条件下,没有一个测试菌株能够将这些化合物激活为诱变产物。在使用先前用苯巴比妥处理过的雄性金黄地鼠肝脏匀浆(S-9组分)的实验中,黄曲霉毒素B1在大肠杆菌和酿酒酵母中均表现出很强的遗传活性,而黄曲霉毒素G1的诱变活性明显较低,且仅在大肠杆菌测试菌株中能检测到。这些结果与黄曲霉毒素G1比黄曲霉毒素B1致癌性和诱变性更低的研究结果相关。