The relationship between cell killing, chromosome aberrations, spindle defects and mitotic delay in mouse lymphoma cells of differential sensitivity to X-rays.
The ultrasensitivity of a subline of L5178Y mouse lymphoma cells to X-rays was thought to result from chromosome structural aberrations which are much more frequent in these cells than in radiation-resistant cells derived from them (Scott, Fox and Fox 1974). However, Ehmann, Nagasawa, Peterson and Lett (1974) in time-lapse photography studies of the sensitive line, concluded that the induction of multipolar mitoses by X-rays might be a more important mechanism of cell killing than chromosome aberrations. We have now shown that at survival levels above about 20 per cent, chromosome structural aberrations which lead to bridges and fragments at anaphase are about four times more frequent than spindle defects. We have confirmed the higher frequency of structural aberrations and spindle defects, and the greater mitotic delay in the X-ray-sensitive than in the X-ray-resistant cell line and have proposed a model which causally relates these end-points to cell killing and DNA repair.
D000705:Anaphase / Q000528:radiation effects; D000818:Animals; D002460:Cell Line; D002470:Cell Survival / Q000528:radiation effects*; D002869:Chromosome Aberrations; D008223:Lymphoma; D008677:Metaphase / Q000528:radiation effects; D051379:Mice; D008938:Mitosis / Q000528:radiation effects*; D008940:Mitotic Index; D013692:Telophase / Q000528:radiation effects; D013997:Time Factors; D014965:X-Rays