Abstract
Repair replication occurs in response to alkylation of DNA in normal human cells and in cells from two patients with the hereditary disease xeroderma pigmentosum (XP). Normal and XP cells perform similar amounts of repair replication after treatment with methyl methanesulfonate (MMS) and N-methyl- N'-nitrosoguanidine (MNNG) indicating that such repair is independent of the biochemical defect in XP (presumably a defect in the initial step of excision repair of UV radiation damage). The results imply that these alkylating agents are similar to ionizing radiation and produce chemical breaks in DNA which then induce repair replication. Repair replication levels in normal and XP cells are similar after nitrogen mustard treatment, but these levels are low and within the capacity of the low residual excision repair in XP cell lines. The chemical mechanisms of nitrogen mustard damage are not resolved in these experiments. At high doses of MMS and MNNG repair replication is inhibited, probably because of enzyme inactivation.
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