DNA-repair kinetics and the sensitivity of cells to X-ray-induced chromosome aberrations: a mouse myeloid leukemia cell line and normal mouse bone marrow cells.
The frequency of X-ray-induced chromosome aberrations in G1 ML-1 mouse myeloid leukemia cells and normal mouse bone marrow cells increased with post-irradiation incubation with the DNA-repair resynthesis inhibitor 1-beta-D-arabinofuranosylcytosine (araC), but the frequency of aberrations in the leukemic cells increased with quite a different time response compared to the normal cells. Irradiated normal mouse bone marrow cells had a rapid increase in the frequency of chromosome exchanges and deletions with increasing araC incubation time, for example, an increase was observed with 0.5 h araC incubation. In contrast, the ML-1 cells did not have a significant increase in aberrations until 1-2 h post-irradiation incubation with araC. These results suggest that the ML-1 cells, per unit time, initially undergo less repair of the X-ray-induced DNA damage that can be converted into chromosome aberrations. We previously showed that the ML-1 cells have a higher frequency of X-ray-induced chromosome aberrations compared to normal cells and the results presented here indicate that a slower rate of repair resynthesis is contributing to the increased sensitivity of the ML-1 cells.
Aardema
M J
MJ
Preston
R J
RJ
D000818:Animals; D001853:Bone Marrow / Q000528:radiation effects; D002453:Cell Cycle / Q000528:radiation effects; D002460:Cell Line; D002869:Chromosome Aberrations / Q000528:radiation effects*; D003561:Cytarabine / Q000494:pharmacology; D004260:DNA Repair / Q000187:drug effects / Q000528:radiation effects; D015470:Leukemia, Myeloid, Acute; D051379:Mice; D014965:X-Rays
D003561:Cytarabine