Abstract
22 nitrofurans were tested for ability to induce revertants of E. coli WP2 and its uvrA- derivative from tryp- to tryp+. All proved to be mutagnic while two furan analogues (lacking the nitro- group) proved to be inactive. Test strains containing exrA- or recA- genes were not induced to mutate, suggesting that mutants arise in the other strains during repair of damage to DNA by the “error-prone” repair system. Two mutant strains isolated from WP2uvrA- on, the basis of resistance to nitrofurazone were not mutated by nitrofurazone or N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) indicating that the ultimate mutagens are likely to be a reduction product rather than the nitrofurans per se. Several of the nitrofurans cause induction of prophage leading to mass lysis in E. coli T44 (λ) a strain which is known to be very sensitive to heat and certain chemicals. Since two nitrofurans which have been reported to lack carcinogenic activity proved to be mutagnic, it is suggested that further assessment of the hazards that medical use of nitrofurans poses to humans should be further evaluated.
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