Potassium chromate potentiates frameshift mutagenesis in E. coli and S. typhimurium.

Possible comutagenic effects of chromate on frameshift mutagenesis were studied in bacterial assays. In these experiments, cells were treated with potassium chromate and 9-aminoacridine either singly or in combination. Results were analyzed to detect synergistic, additive and antagonistic responses. Data from these investigations show a clear potentiation of 9-aminoacridine-induced mutagenesis in the presence of chromate in S. typhimurium strain TA1537. Results from cell viability assays shows that the effect is not due to a toxicity artifact. Similar results are obtained in E. coli strains 343/358 (repair-proficient parental strain), 343/415 (recA-deficient), and 343/435 (mismatch-repair-deficient). These data indicate the neither induction of recA-protein nor inhibition of mismatch repair is involved in the action of chromate. In E. coli strain 343/447 (DNA polymerase I deficient), the potentiation was observed at lower concentrations of chromate. This finding suggests that polymerase I functions in recovery of cells from 9-aminoacridine-induced DNA damage and that its absence allows some of this damage to be dealt with in a manner which promotes mutagenesis in the presence of chromate. One possible explanation of these findings is that chromate and 9-aminoacridine react chemically to produce a unique mutagen and that damage caused by this mutagen is repaired via some excision process. However, no reaction between chromate and 9-aminoacridine could be detected by TLC under conditions similar to those in the bacterial assays, even at very high concentrations of both agents. Thus, it seems most likely that the potentiation is due to some action of chromate on repair and/or replication at sites of 9-aminoacridine intercalation. Chromate appears, then, to have significant comutagenic actions in bacterial systems.