Mutations induced by substituted quinolines in ultraviolet-irradiated bacteria.

The drugs griseofulvin (10 μg/ml), nalidixic acid (0.05 μg/ml), quinine dihydrochloride (50 μg/ml), quinine ethylcarbonate (50 μg/ml), quinine urea hydrochloride (50 μg/ml), quinine lactate (50 μg/ml), and pamaquine (50 μg/ml) were chosen for laboratory studies. The minimal inhibitory concentration of the drug was used for determining the range of drug concentration needed to produce "mutational synergism" with ultraviolet radiation. Forward mutation from streptomycin sensitivity to resistance was used as a marker for mutagenicity. No stimulatory or inhibitory effects were noted on viable counts and mutation frequency, when the drugs were added (20-60 μg/ml) to the growth medium of unirradiatedEscherichia coli HCR(+), HCR(-), and irradiated HCR(-) strains. These drugs increased mutation frequency and lethality of irradiated HCR(+) bacteria. Incorporation of adenine (6 μm) into the minimal expression medium reverses the mutagenic effect of chloroquine. Chloroquine (50 μg/ml) did not interfere with the photoactivation of irradiated HCR(+) cells. Our findings suggest that these chemicals selectively interfere with excision-repair.