Chinese hamster cells were X irradiated either aerobically or hypoxically, after flushing with nitrogen plus carbon dioxide. In agreement with earlier data, for asynchronous cells, the oxygen enhancement ratio (OER) was approximately three. If the sulfhydryl-binding agent N-ethylmaleimide (NEM) was present during or immediately after irradiation, the principal effect was a pronounced decrease in the extrapolation number of the survival curve of NEM-treated cells compared to nontreated cells. This was observed with hypoxic as well as aerobic cells and the OER for NEM-treated cells was also about three. For NEM treatments which were essentially nontoxic, NEM acts synergistically with X rays, suggestive of an inhibition by NEM of a cell's ability to repair sublethal damage. For synchronous cells obtained by mitotic selection, a result consistent with the above was obtained; a dose three times as large was necessary to reduce survival to the same level for hypoxic cells as for aerobic cells, whether or not the cells were treated with NEM. Thus the OER was independent of NEM treatment throughout the cell cycle, with the possible exception of mitosis which could not be studied with the methods used. It is concluded that the action of NEM at low concentrations (0.75 μM) is largely independent of oxygen tension. Oxygen acts to produce more damage per unit dose in the cell while NEM sensitizes apparently by preventing the repair of sublethal damage.

Synchronized Chinese hamster cells in vitro were used to examine the stage dependence of the induction of polyploidy by X-irradiation. The data obtained from various experiments, including cells that were in the G 1 and S stages of the cell cycle only, showed that polyploid cells can be induced only when they are irradiated in G 1 . This finding is supported by autoradiographic studies, in which no induced polyploid cells were labeled with <tex-math>${}^{3}{\rm HTdR}$</tex-math>, and by the fact that chromosome aberrations were observed only in these polyploid cells.

The magnitude of mitotic delay and the incidence of chromosomal aberrations depend upon the stage at which irradiation occurs in the cell generation cycle of synchronized Chinese hamster cells in vitro. Because cysteamine has a differential protective effect upon cell lethality during the cell cycle, the dependence of its protective effect against mitotic delay and chromosomal aberrations upon cell cycle position was investigated. The results show that cysteamine-treated cells have a pattern for radiation-induced mitotic delay and chromosomal aberrations similar to that for untreated cells, except that the dose required is much higher. The fact that a differential effect was not observed may be because the degree of synchrony was not sufficient to permit the detection of small differences. However, the magnitude of the dose-modifying factor for cysteamine differed in each assay from those previously reported for lethality. The dose-modifying factor for mitotic delay was about 2.5 throughout the cell cycle, for single-hit aberrations it was about 8, and for two-hit aberrations, about 5.