Alkaline sucrose-density gradient results indicate that aerobic irradiation of log phase E. coli B/r CSH is 4.5 times more effective than anoxic irradiation in producing single-strand breaks in DNA. If 0.02 M EDTA, presumed to inhibit the rejoining enzyme, is present during irradiation, the yield of breaks is increased 6-fold in air and 10-fold in nitrogen, thus aerobic conditions are still more effective than anoxic in producing breaks. Holding bacteria at 0°C in buffer after aerobic or anoxic radiation resulted in 80-90% of the observed breaks being rejoined. Since rejoining takes place during irradiation, the yield of breaks is dose-rate dependent. The oxygen effect on single-strand breaks in log phase E. coli B/r may be related to radiation survival: however, survival is not improved by lowering the dose rate nor by postirradiation holding at 0°C conditions which result in the rejoining of breaks. Holding irradiated bacteria in buffer at 37°C results in only a small amount of rejoining, while considerable loss of label takes place due to DNA degradation. Holding at 37°C in growth medium, however, results in DNA degradation accompanied by a marked increase in molecular weight of TCA-insoluble DNA.

Dose-survival curves of four strains of E. coli-B/r <tex-math>${\rm hcr}^{-}\ {\rm try}^{-},\ {\rm B}_{{\rm s}-1}$</tex-math>, B/r CSH, and <tex-math>$15{\rm T}^{-}$</tex-math>-were obtained in the presence and in the absence of nontoxic levels of several thiol-binding agents-N-ethylmaleimide (NEM), iodoacetamide (IA), and hydroxymercuribenzoate (HMB). The degree of radiosensitization by these agents was estimated from the increase in slope of the dose-survival curve, under anoxic and aerobic conditions. Chemical sensitization of both radioresistant and radiosensitive strains of bacteria with the thiol-binding enzyme poisons NEM, IA, and HMB has been observed. NEM sensitized only under anoxic conditions, IA sensitized under both anoxic and aerobic conditions, although to a much greater extent aerobically, and HMB sensitized only under aerobic conditions. The formation of long-lived radiolytic products toxic to bacteria is observed in sensitization by IA. When sensitization occurs, the magnitude of the dose-modifying factor is equal to or greater than the oxygen enhancement ratio. Inhibition of an energy-requiring enzymic repair process does not seem to be involved as a primary mechanism of sensitization. Interference by thiol-binding agents with a "rapid repair" process which is different from the usual "enzymic repair," and which operates in radiosensitive as well as in radioresistant bacteria, is suggested.