Add time:08/09/2019         Source:sciencedirect.com

Although ICR 191 has been reported to act as an intercalating and alkylating mutagen in prokaryotes, it is not clear that it acts as a mutagen in eukaryotes. Therefore, we looke for evidence that this acridine half-mustard (cas 17070-44-9) induces DNA repair in haploid Rana pipiens or in diploid human fibroblast cell lines. We measured repair autoradiographically as unscheduled DNA synthesis. Concentrations of 10−5 to 10−7 M ICR 191 failed to induced repair as determined by two criteria. Of 400 nuclei examined for each concentration, the percentage of labelled nuclei did not increase during or up to 18 days after treatment. Secondly, a new class of lightly labelled nuclei did not appear. However, by these criteria, the mutagen and carcinogen, N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) stimulated unscheduled DNA synthesis in both frog and human fibroblast populations at the tested concentrations (10−4 to 10−6 M). The MNNG-induced repair indicated that this autoradiographic technique is sufficiently sensitive to detect unscheduled DNA synthesis, and that frog cells, like human cells, are competent to perform excision repair. Intracellular localization of ICR 191 was examined by fluorescence microscopy and showed preferential interaction with the lysosomes rather than the genome of haploid frog cells. The repair and fluorescence studies indicate that the primary intracellular localization of ICR 191 takes place outside the genome in these eukaryotic cells.

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