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Activity of quinolones in the Ames Salmonella TA102 mutagenicity test and other bacterial genotoxicity assays.

机译:喹诺酮类药物在Ames沙门氏菌TA102致突变性试验和其他细菌遗传毒性试验中的活性。

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摘要

Eight quinolones were examined for their bacterial mutagenicity in the Ames Salmonella TA102 assay and for their effects in other bacterial genotoxicity assays. In the quantitative Ames plate incorporation assay, all eight quinolones induced His+ deletion reversion in Salmonella tester strain TA102, with maximum reversion observed at about two to eight times the MIC. The quinolones also induced the SOS response. At quinolone concentrations close to the MIC, SOS cell filamentation gene sulA was induced in sulA::lacZ fusion strain Escherichia coli PQ37. RecA-mediated cleavage of lambda repressor in lambda::lacZ fusion strain E. coli BR513 was measurable at about 10 times the MIC, though no induction occurred at 20 micrograms of nalidixic or oxolinic acid per ml. Genotoxicity of quinolones also was observed in the Bacillus subtilis DNA repair assay, in which the mutant strain M45 (recA) was more susceptible to quinolones than its parent strain, H17 (rec+). The results from these analyses indicate that quinolones induce SOS functions and are mutagenic in bacteria; these properties correspond to their antimicrobial activities.
机译:在Ames Salmonella TA102分析中检查了八个喹诺酮类细菌的致突变性,并在其他细菌遗传毒性分析中检查了它们的作用。在定量Ames平板掺入试验中,所有八种喹诺酮类药物均可引起沙门氏菌测试菌株TA102的His +缺失逆转,在MIC的2至8倍处观察到最大逆转。喹诺酮类药物也引起SOS反应。在接近MIC的喹诺酮浓度下,在sulA :: lacZ融合菌株大肠杆菌PQ37中诱导了SOS细胞细丝化基因sulA。 RecA介导的λ:: lacZ融合菌株大肠杆菌BR513中λ阻遏物的裂解可在MIC的10倍下测得,尽管每毫升20毫克萘啶酸或草酸无诱导作用。在枯草芽孢杆菌DNA修复试验中也观察到喹诺酮类的遗传毒性,其中突变菌株M45(recA)比其亲本菌株H17(rec +)对喹诺酮类药物更敏感。这些分析的结果表明,喹诺酮类药物具有SOS功能,并且在细菌中具有致突变性。这些性质与其抗菌活性相对应。

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