Is N2O-dependent damage 'fixed' by action of the recA locus?

Nitrous oxide (N2O) is often a radiation sensitizer of procaryotic cells, although it has little or no effect in recA- strains of E. coli and Saccharomyces. Here we test the hypothesis that N2O-dependent damage is in itself not lethal, but that lethality occurs when this damage is incorrectly repaired by the recA+ strains. Because sensitization by N2O requires the radiolytic production of H2O2, the hypothesis can be tested with reagent H2O2. If the 'inaction' of the recA locus prevents N2O sensitization in the recA- strains, then those strains should not be sensitized by reagent H2O2. Our data show that all these strains, including the recA+ parent, are efficiently sensitized by reagent H2O2 in N2 and also in N2O; thus or data do not support that hypothesis. We propose instead that the correlation between N2O sensitization and the recA- genotype occurs because of the inherent anoxic sensitivity of the recA- strains; the doses used to assay survival, and thus to test for sensitization by N2O, are simply too low to produce sufficient H2O2 for sensitization to occur.