1-beta-D-Arabinofuranosyl cytosine (araC), a pyrimidine nucleoside analog used in the treatment of malignant tumors [1, 2], inhibits ultraviolet repair of DNA in a reversible manner. The inhibition occurs during the resynthesis-ligation step and is apparent at all sites undergoing repair. By use of araC it was possible to substantiate the reported observation that the initial velocities of ultraviolet repair are dose dependent and that hamster and human cells are more efficient that mouse cells in excising DNA damage after fluences of less than 50 J/m2. araC does not strongly inhibit gamma-ray-induced repair, although alkali-labile sites are removed more slowly in araC-treated cells. Repair of damage to DNA by N-methyl-N-nitrosoguanidine, mitomycin C, 4-nitroquinoline oxide and 8-hydroxyquinoline is strongly inhibited by araC.
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