Chromium(VI) and apparent phenotypic reversion in Salmonella TA100

Abstract

After treatment with potassium chromate at concentrations causing ultramicroscopic cellular lesions, a significant proportion (up to 75%) of TA100 colonies fail to replicate on fresh minimal plates containing biotin. This suggests that chromium(VI) may not always induce his − reversion to his + in Salmonella TA100. The terms ‘false’ or phenotypic reversion have been used to distinguish such instances from ‘true’ or genotypic reversion, where progeny his + cells readily grow on biotin replica plates. Results of the present study indicate that the majority of chromate-exposed colonies, initially scored as his −, are identifiable as his + after 24 h culture on nutrient agar. Moreover, chromate exerts a cytostatic effect on TA100 since early colony development is suppressed at high chromate concentrations. A gradual chemical reduction of chromium(VI) ions by normal media compounds is probably responsible for the re-emergence of colony growth during prolonged incubation of test plates. Thus, temporary growth inhibition at high chromate concentration appears to be responsible for most of the non-replicating colonies detected in mutagenicity assays of chromium(VI).