SV40-transformed normal, xeroderma pigmentosum (XP) and Fanconi's anemia (FA) fibroblasts have distinct repair capacities for monoadducts and DNA interstrand cross-links produced by exposure to near-UV (320–400 nm) light in the presence of 8-methoxypsoralen or angelicin. Excision repair of monoadducts occurred rapidly in normal and FA cells after exposure but not in XP cells. Cross-links were repaired in normal cells with a tv2 of about 10 h but not in XP or FA cells. When the total number of adducts induced by 8-methoxypsoralen in normal cells was kept constant, the amount of repair replication decreased as the ratio of cross-links to monoadducts increased. This suggests either that cross-link repair is significantly different from monoadduct repair, involving smaller patches and a much slower rate of patching or that cross-links can inhibit monoadduct repair. Our results show that XP group A and FAH12 cell lines are deficient in cross-link repair. The data also suggest that the mechanism of cross-link repair in human cells involves several enzymes and that different ones may be deficient in XP and FA cells.


This work was supported by the United States Department of Energy (Contract No. DE-AC03-76-SF01012) and National Cancer Institute Radiation Biophysics Training Grant 5A32 CA09272-04 (D. C. G.).

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