Cell cycle‐related variations in UV damage and repair capacity in chinese hamster (CHO‐K1) cells

Abstract

UV damage to CHO cell DNA, measured by formation of thymine‐containing dimers, increases from mitosis to early S phase. Computer simulation of UV absorption by the DNA of an idealized CHO cell at different stages in the cell cycle resembles the cycle dependence of UV damage. Incision at UV damage sites, measured by the accumulation of breaks in preexisting DNA during 30 minutes' post‐irradiation incubation with the DNA synthesis inhibitors 1‐β‐D arabinofuranosylcytosine and hydroxyurea, increases from mitosis to interphase. Analysis of the dose dependence of DNA break accumulation indicates that both the affinity of the endonuclease for dimer sites and the maximum enzyme activity at saturating levels of dimers are significantly lower in mitosis than in interphase. The killing of CHO cells by UV is enhanced if repair is temporarily inhibited by ara C. The DNA gyrase inhibitor novobiocin prevents UV‐induced incision.