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Laboratory of Radiobiology, University of California, San Francisco, California 94122
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)-1-nitrosourea; they show normal repair after exposure to agents such as N-methyl-N'-nitro-N-nitrosoguanidine. These results allow agents to be classified according to whether or not xeroderma pigmentosum cells respond normally to them and illustrate the values and limitations of the use of xeroderma pigmentosum cells or measurements of DNA repair as test systems for carcinogens.
1 Work performed under the auspices of the U. S. Atomic Energy Commission.
Received 8/21/72. Accepted 11/ 2/72.
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