UV-Type Repair after Chemical Damage

A report of our experiments with jV-acetoxy-AAF has appeared elsewhere (Setlow and Regan, 1972). It is an agent that should hold considerable interest for photobiologists. We found that treatment of human skin-cell cultures with 0.7 xm JV-acetoxy-AAF resulted (in the BrUra photolysis assay) in repair events indistinguishable from those induced by irradiation of the cells with 50 ergs/mm of 254-nm UV (Fig. 9). In terms 

FIGURE 9. Molecular-weight shifts seen in normal-cell and XP tumor-cell DNAs on alkaline sucrose gradients after treatment with the carcinogen jV-acetoxy-AAF. Note similarity to UV repair (Fig. 5). (From Setlow and Regan, 1972.) 

FIGURE 10. J llMw) response to 313-nm radiation after treatment with ICR-170 in normal and XP cells. Note similarity to jV-acetoxy-AAF (Fig. 11) and UV repair (Fig. 6). 

ICR-170 is an acridine with one nitrogen mustard group. It has been employed as an antitumor agent (Creech et al., 1972). In our repair assay, this agent induced repair events similar although not identical to those induced by jV-acetoxy-AAF (Fig. 10). ICR-170 differed from jV-acetoxy-AAF in that the size of the repaired regions with ICR-170 was smaller (approximately ten BrUra residues) than those with jV-acetoxy-AAF (approximately 25 BrUra residues). Nevertheless, ICR-170 clearly induces UV-type repair in normal cells and, like jV-acetoxy-AAF, defective repair in XP cells (see Section VI). 

XERODERMA PIGMENTOSUM AND UV-TYPE REPAIR AFTER CHEMICAL DAMAGE TO DNA 

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