The incorporation of [3H]thymidine and [3H]deoxyguanosine into DNA was studied during DNA repair in mouse skin cells treated with the skin tumor initiator N-methyl-N′-nitro-N-nitrosoguanidine. At high, toxic levels of N-methyl-N′-nitro-N-nitrosoguanidine, repair (incorporation of the precursor into DNA which had not replicated) was demonstrated with both precursors. At lower, less toxic doses of the carcinogen, repair could not be demonstrated with [3H]-thymidine, but it was clearly demonstrable with [3H]deoxyguanosine. Thus, we are apparently observing two kinds of DNA repair, one in which a single base (in this case, guanine) replaces a base lost by Chemical or enzymatic depurination and the second in which more than one base is replaced, indicating synthesis of longer stretches of DNA after extensive enzymatic excision. The guanine-specific repair shown at relatively nontoxic dose levels of N-methyl-N′-nitro-N-nitrosoguanidine may be more relevant to the survival of cells than the repair demonstrated with [3H]thymidine at higher doses.

This content is only available via PDF.