Mutagenic and cytotoxic effects of oxygen free radicals generated by methylviologen (paraquat) on Escherichia coli with different DNA-repair capacities.

Investigations were carried out to examine the mutagenic and cytotoxic effects of oxygen free radicals on E. coli. E. coli B strains with different DNA-repair capacities were exposed to methyl viologen, commonly called paraquat (1,1'-dimethyl-4,4'-bipyridinium dichloride, MV), which has been shown to act as an intracellular generator of superoxide radicals. The results obtained were as follows: The cytotoxicity of MV in E. coli was dioxygen-dependent and due to the extent of intracellular generation of superoxide radicals. Cells containing higher levels of superoxide dismutase were more resistant to the toxic effect of MV. The cytotoxicity of MV was greater in DNA repair-deficient E. coli, Bs-1(exrA uvrB), NG30(recA) and R15(polA), than in DNA-repair-proficient strains (B/r and H/r30) and Hs30 (uvrB). MV was found to be mutagenic to E. coli H/r30 and Hs30 under aerobic conditions. The mutation frequencies to streptomycin resistance and to arginine prototrophy increased with the dose of MV in both strains. However, E. coli NG30 was unmutable by MV. The mutation induction did not occur under anaerobic conditions. The expression of the umu operon in E. coli was induced by MV under aerobic conditions. From these results, it was concluded that superoxide radicals intracellularly generated by MV include DNA damage, which causes cytotoxicity and mutation induction in E. coli, and that DNA damage induced by oxygen radicals is repairable by at least recA, polA and exrA(lexA) gene-controlled mechanisms.