Defective Repair of Ultraviolet- and Gamma-ray-damaged DNA in Fanconi's Anaemia

Publisher Website
Google Scholar
Abstract
Using a sensitive host-cell reactivation technique for irradiated virus, a deficiency in the repair of DNA damaged by either UV or gamma-rays (.gamma.) was detected in fibroblasts from one of the FA [Fanconi''s anemia] lines reported to have normal t'' [5,6-dihydroxydihydrothymine] excision at the levels of .gamma. induced damage employed. Unirradiated and irradiated suspensions of adenovirus type 2 (Ad 2) were assayed for their ability to form viral structural antigens (V Ag) in human fibroblast cells infected in monolayer. The frequency of V-antigen-positive cells was similar for both the FA and the normal lines when infected with unirradiated virus, but the frequency of V-antigen-positive cells was considerably lower in the FA fibroblasts than in the normal when relatively large doses of UV were given to the virus. A similar reduction was also found for FA fibroblasts when relatively large .gamma. doses were given to the virus. The reduced V-antigen survival for FA after relatively high doses of either UV or .gamma. indicates a defective DNA repair mechanism for this cell-line. The fact that no deficiency in t'' excision was detected in this FA line may suggest that it is defective in the repair of some other .gamma.-ray-induced lesion.
Keywords