• 1 January 1984
    • journal article
    • research article
    • Vol. 44  (10) , 4396-4402
Abstract
The repair of bleomycin-damaged DNA was examined in human fibroblasts isolated from patients having the disease xeroderma pigmentosum (XP). In normal fibroblasts, the appearance of low-MW DNA was observed in the presence of increasing amounts of the drug. The studies in XP fibroblasts produced results which differed from those obtained in normal cells in 2 ways. Prelabeled XP cells from most complementation groups contained more low-MW DNA than observed in the other human fibroblasts examined. When XP cells were exposed to low doses of bleomycin, the low-MW DNA disappeared, suggesting induction of a repair process. If the XP cells were exposed to bleomycin in the presence of hydroxyurea and 1-.beta.-D-arabinofuranosylcytosine, the disappearance of low-MW DNA was not observed; instead, a normal dose response to the drug was observed. XP cells evidently show an induced repair response following bleomycin treatment. Blocking DNA chain elongation uncovers normal incisions in bleomycin-treated DNA.

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