Arrest of irradiated G1, S, or G2 cells at mitosis using nocodazole promotes repair of potentially lethal damage.
The ability of synchronized Ehrlich ascites tumor cells, irradiated in G1, S, and G2 phases, to repair potentially lethal damage when arrested at mitosis by using 0.4 microgram/ml nocodazole, a specific inhibitor of microtubule polymerization, has been studied. Cells irradiated in these phases were found to repair potentially lethal damage at mitosis. The extent of this repair was similar to that observed for cells irradiated at the same stages in the cell cycle but allowed to repair potentially lethal damage by incubating in balanced salt solution for 6 hr after X irradiation.
D000818:Animals; D001562:Benzimidazoles / Q000494:pharmacology*; D002286:Carcinoma, Ehrlich Tumor; D002470:Cell Survival / Q000528:radiation effects; D004260:DNA Repair; D004273:DNA, Neoplasm / Q000528:radiation effects; D004307:Dose-Response Relationship, Radiation; D007399:Interphase / Q000528:radiation effects*; D051379:Mice; D008870:Microtubules / Q000187:drug effects; D008938:Mitosis / Q000187:drug effects*; D015739:Nocodazole
D001562:Benzimidazoles; D004273:DNA, Neoplasm; D015739:Nocodazole