Relationship of Enhanced Survival during Confluent Holding Recovery in Ultraviolet-Irradiated Human and Mouse Cells to Chromosome Aberrations, Sister Chromatid Exchanges, and DNA Repair

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Abstract
The relationship among cellular recovery from UV damage, cytogenetic changes, and DNA repair was studied in density-inhibited cultures of mouse 10 t1/2 [half-life] cells and human diploid fibroblasts. Both cell types showed similar UV sensitivities to cell killing and a similar enhancement in survival when subculture to a low density was delayed for 24-48 h after irradiation (potentially lethal damage repair). Excision repair as measured by the loss of endonuclease-sensitive sites was biphasic and much slower in the mouse cells: 30% were removed in the first 24 h compared with 60% removed in the first 5 h in the human cells. More than 5 times as many excision-induced DNA strand breaks as measured by alkaline elution were detected in the human as compared with the mouse cells. DNA protein crosslinks were removed with a t1/2 of 30 h after 10 j/m2 UVL. UVL induced few chromosomal aberrations in the human cells as compared with mouse cells. The frequency of induced sister chromatid exchanges and the pattern of their decline during recovery were similar in both cell types; the kinetics of this decline was similar to that observed for the removal of DNA-protein crosslinks, and slowly removed endonuclease-sensitive sites. Chromosome aberrations, however, correlated with rapidly removed endo sites and DNA strand breaks and appeared to reflect the number of residual pyrimidine dimers in DNA at the time of its replication.

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