Reversion of the hisC3076 frameshift marker of Salmonella typhimurium has been measured following treatment of cells in growth and non-growth media with 9-aminoacridine (9AA). By varying the carbon source present in a defined medium, it has been shown that mutagenesis is reduced close to the spontaneous level in the presence of glucose whilst significant reductions are also observed with glucosamine, mannose, mannitol, fructose or glucose 6-phosphate. Intermediate mutant yields are observed when lactic acid or glycerol are present, whereas any one of a further group of carbon sources (gluconate, arabinose, ribose, succinate or casein hydrolysate) permit relatively large numbers of mutants to be recovered. Interestingly, when any one of these "high yield" carbon sources is supplemented with glucose the strong inhibitory effect characteristic of glucose is again observed. On the basis of these results, it can be concluded that inhibition of 9AA-induced reversion by a carbon source is not an exclusive property of glucose, although when more than one carbon source is present the inhibitory effect of glucose predominates. Possible explanations for these findings include the active exclusion of 9AA from cells as a direct consequence of glucose transport across the cell membrane. To address this possibility, cells were pre-grown in verapamil, a calcium channel antagonist which is known to increase the mutagenicity of various 9-anilinoacridine derivatives in S. typhimurium. We found that glucose inhibition of 9AA-induced mutagenesis was not relaxed to any significant extent following treatment with verapamil. In a further experiment, two glucose analogues (2'-deoxyglucose and methyl-D-glucoside) known to be actively transported into the cell but not metabolised past the first phosphorylation step were used. These analogues inhibit the transport into the cell of several types of molecules, but since they do not significantly depress 9AA mutagenesis it seems unlikely that blockage of 9AA transport across the cell membrane can be invoked to explain the inhibitory effect of glucose on 9AA mutagenesis. An alternative explanation based on glucose-mediated repression of an error-prone, mutation-generating, DNA-repair process is presented.