<p> The variation in sensitivity of L60T cells to gamma rays has been studied as a function of position in the cell division cycle. For a dose range of 0-12,000 rads, no significant variation was found for mitotic delay. Such was not the case for sensitivity to cell killing, which was found to increase as the cells passed from G1 through S to G2 of the division cycle. The results of mitotic delay are in disagreement with results published by other workers although the survival data agree with previous reports for a similar cell line. Results reported in connection with cell cycle determinations and mitotic delay suggest that the existence of a repair cycle operating concurrently with the normal cell cycle may be postulated. The theoretical treatment of mitotic delay given by Lea is examined and is not found to describe adequately the present results. Finally, the evidence reported here suggests that mitotic delay and radiation lethality are not separate manifestations of the same phenomenon. Experimental materials for further investigation into the repair processes involved are suggested.</p> / Thesis / Master of Science (MSc)

The requirement of DNA synthesis for the release of Ɣ-radiation-induced mitotic inhibition in mammalian cells has been studied. Mammalian cells in which DNA synthesis had been inhibited by treatment with fluorodeoxyuridine (FUdR) were not released from radiation-induced mitotic inhibition until the FUdR block was removed. After removal of the block, mitotic figures reappeared, but only after a time equivalent to the usual mitotic delay caused by the particular radiation dose employed. This suggests that repair of the mitotic inhibition lesion can not proceed unless the pathway for DNA synthesis is intact. Further evidence for the requirement of DNA synthesis in the release of mitotic inhibition came from the observation of radiation-induced synthesis of DNA during G₂, a stage in the cell cycle normally not associated with such synthesis. / Thesis / Master of Science (MSc)