Chromosome-type exchange aberrations are induced by inhibiting repair of UVC-induced DNA lesions in quiescent human lymphocytes.
Human lymphocytes in the quiescent stage were UVC-irradiated and then incubated for 90 min in the presence of the DNA-repair inhibitor ara-C. The cells were then cultured and analyzed for chromosome aberrations. A single treatment with UVC or ara-C gives rise to a very low yield of dicentrics, whereas the combined treatment can induce a high frequency of these chromosome-type aberrations. The yield in the combined treatment is approximately proportional to the square of the UVC fluence in the range 1-3 J/m2. In addition, the experiments demonstrate that synergistic effects arise when cells are treated with UVC + ara-C and then exposed to X-rays. The results can be explained on the assumption that the UVC + ara-C treatment induces DNA double-strand breaks which, to the first approximation, are randomly distributed over the chromosomes. These breaks are able to interact with each other as well as with X-ray-induced DNA double-strand breaks to form a chromosome-type exchange aberration.
Holmberg
M
M
National Institute of Radiation Protection, Stockholm, Sweden.
Gumauskas
E
E
D002869:Chromosome Aberrations; D003561:Cytarabine / Q000494:pharmacology; D004260:DNA Repair / Q000187:drug effects / Q000502:physiology*; D004307:Dose-Response Relationship, Radiation; D006801:Humans; D066298:In Vitro Techniques; D008214:Lymphocytes / Q000378:metabolism / Q000528:radiation effects*; D016192:Resting Phase, Cell Cycle / Q000528:radiation effects; D014466:Ultraviolet Rays; D014965:X-Rays
D003561:Cytarabine