On the mutagenicity of nitrofurans

UV (254 nm)-irradiated Tr phages infecting excision-repair-proficient E. coli cells undergo host-cell reactivation (HCR). Typically, the resulting survival curve is of a hetero-component type, i.e. extrapolation of the shallower curve component to zero UV dose gives ordinate values p < 1. This characteristics is accentuated if HCR is inhibited by UV irradiation of host cells prior to phage infection, or by the presence of caffeine or acriflavine. With increasing strenght of the inhibitory condition, p decreases and the slope of the steeper curve component increases, but the slope of the shallower curve component changes very little. In contrast, single-component curves are observed for Tr infecting excision-repair-deficient host cells, or for Tr undergoing photoenzymatic repair in these cells either with or without inhibition by caffeine or preirradiation of host cells. This indicates that throughout the population UV lesions are photorepaired or photorepair-inhibited independently of one another.Discussion of various possible interpretations of the hetero-component curves in the case of HCR suggests the existence of two modes of excision repair, one of them leading to a high degree of interdependence between repair events within individual phage particles. This mode of repair, which determines the slope and position of the shallower curve component, requires within an infected cell the occurrence of a “critical event”, whose probability is considerably lower than i and decreases with the strength of HCR inhibition. The other mode, leading to independent repair events, is of minor importance under our usual plating conditions, but plays a predominant role in liquid-holding recovery of the phage.