The simple reversible intercalating agents isopropyl-oxazolopyridocarbazole and 9-aminoacridine have been found to induce frameshift -1 mutations at a much lower level in Salmonella typhimurium delta uvrB TA 1537 than in the uvr+ wild type TA 1977 strain. This phenomenon can neither be explained by differential cytotoxicity of the drug nor by selective permeation and accessibility to intercalating sites to bacterial DNA. These finding indicate that the lower mutagenicity of intercalating agents in the delta uvrB strains does not result from nonspecific phenotypic modifications of parameters which control the mutagenesis. That leads to the hypothesis that in agreement with the Streisinger's model, the excision repair system could be directly involved in the appearance of frameshift mutations.