The effect of superoxidc anion (02-) on killing of cells was studied. E. coli was killed by a non-enzymatical 02--generating system, i.e. a phenazine methosulfate (PMS)-NADH system. Both polA and recA repairdeficient mutants were more sensitive to 02 _ than wild type cells. Furthermore, using the polA mutant strain, it was clearly shown that incubation in growing medium increased survival, indicating the involvement of a rec-dependent repair system. It was concluded that the direct cause of cell death induced by 02 was DNA damage. When a scavenger of the active oxygen, such as superoxide dismutase (SOD) or catalase, was present in the reaction buffer during 02 _ treatment, the survival of cells increased. Of especial note, cells were completely protected by addition of catalase. It was suggested that H2O2 produced from 02-and H2O was a molecule more toxic to E. coli cells than the 02-itself in this system. When SOD and catalase were induced inside cells by adding methylviologen in the medium, a protective effect against 02-appeared. Cells treated with methyl-viologen were also resistant, although slightly, to aerobic Y-ray irradiation, suggesting that the scavenger of active oxygen in cells was partly responsible for protection against f-ray irradiation. It is deduced that 02-and/or H2O2 generated in cells may be one of the causes of cell damage by aerobic C -ray irradiation.The presence of oxygen during irradiation with ,-rays or X-rays enhances the lethality to living organisms. Such a phenomenon, called the oxygen effect, has been suggested to be caused by the active oxygen molecules such as 02-, OH', H2O2, 102, which are known to be generated in H2O when irradiated under the aerobical condition. There are many reports which indicate that the active oxygen molecules play toxic roles in biological systems (1-3). Concerning the cause of the oxygen effect, however, it is unclear which species of the active oxygen molecule is responsible for the enhancement of the cell damage. Involvement of 02_ 477