Repair of Potentially Lethal Damage in X-Irradiated HeLa Cells1

Abstract

Although it has been known for several years that mammalian cells cultured in vitro are able to repair sublethal damage from ionizing radiations (1), only a few attempts have been made to examine the capacity of these cells to repair damage which is potentially lethal-that is, damage which ordinarily causes cell death, but whose expression can be prevented by appropriate postirradiation treatment. In contrast, numerous studies have been concerned with modifications of the survival of irradiated microorganisms by various postirradiation treatments, such as incubation at suboptimal temperatures (2-4) or in minimal medium (3, 4), or treatment with inhibitors of protein synthesis (5, 6). These have led to the conclusion that postirradiation repair processes occur in microorganisms. The few studies carried out with cultured mammalian cells suggest that similar repair processes may also occur in these cells. Thus, it has been observed that incubation at low temperature can cause either an increase (7, 8) or a decrease (9, 10) in cell survival, although there may be no effect except a delay in the repair of sublethal damage (11). Similarly, supplementation of the culture medium with a number of complex substances has been reported to enhance cell survival following exposure to ionizing radiation (12-18). Finally, postirradiation treatment of cells with inhibitors of RNA, DNA, or protein synthesis has been found, in some instances, to alter cell survival (8, 19, 20). While studying cyclical fluctuations in radiation sensitivity with the synchronous HeLa S3 system, it was observed that postirradiation treatment of cells with several agents caused significant alteration in cell survival. The results of an investigation