Town, Smith and Kaplan (1972) reported that the yield of DNA single-strand breaks (SSB) in E. coli is largely independent of the presence of molecular oxygen during irradiation. They suggested that the oxygen enhancement ratio (o.e.r.) normally observed is due to the presence of an ultrafast repair mechanism acting (in bacterial cells) mainly on anoxically-produced breaks. To determine whether similar mechanisms exist in mammalian cells, we carried out comparable experiments on two cell-lines, one from Chinese hamster, the other from mouse. Both heat inactivation and chemical inhibition were treatment inactivated all the enzymatic processes assayed, it did not alter the o.e.r. for SSB production, which remained about 3-0. The presence of sodium cyanide, hydroxyurea, iodoacetic acid, EDTA and quinacrine all failed to alter significantly the o.e.r. Isolated nuclei also demonstrated the full o.e.r. For these cell-lines at least, ultrafast reprir does not seem to exist. Isolated Adenovirus 2, which presumably lacks enzymic activity, demonstrated an o.e.r. of 3-6 for SSB production. From these results and others it seems unlikely that the so-called ultrafast enzymic repair is a general phenomenon accounting for the o.e.r. in a wide range of biological systems. Rather, the o.e.r. for SSB seems to result from differences in the direct physico-chemical effects of radiation under aerobic and anoxic conditions in most organisms.