DNA repair with purines and pyrimidines in radiation- and carcinogen-damaged normal and xeroderma pigmentosum human cells.

Repair replication of DNA in cells exposed to UV, X-rays, or chemical carcinogens involves incorporation of both purine and pyrimidine precursors. Previous reports stating that purines are not involved in repair must be due to insufficient resolution in the reported experiments. Hypoxanthine was more efficiently incorporated by repair replication than other precursors such as adenine, deoxyadenosine, and guanine. Hydroxyurea did not inhibit hypoxanthine incorporation by repair replication. Cells from patients with the hereditary high-cancer disease xeroderma pigmentosum show reduced repair after exposure to UV, 4-nitroquinoline 1-oxide, and 1,3-bis(2-chloroethyl)-l-nitrosourea; they show normal repair after exposure to agents such as jV-methyl-TV'-nitro-j'v'-nitroso-