Antibiotic resistance and enhanced insecticide catabolism as consequences of steroid induction in the gram-negative bacterium Comamonas testosteroni.

The effects of steroid induction on antibiotic resistance against the fungal steroid fusidic acid (ramycin; 16-(acetyloxy)-3 alpha,11 alpha-dihydroxy-29-dammara-17(20), 24-dien-21-oic-acid) as well as on carbonyl reduction and degradation of the novel anti-insect agent NKI 42255 (2-(1-imidazolyl)-1-(4-methoxyphenyl)-2-methyl-1-propanone) were studied in the Gram-negative soil bacterium Comamonas testosteroni strain ATCC 11996. Cells grown with testosterone as inducing agent showed a 5-6-fold elevation of antibiotic resistance against the fungal steroid fusidic acid. Furthermore, testosterone induction caused a faster uptake and different metabolism of the anti-insect agent NKI 42255 compared to control cultures, revealing carbonyl reduction of the substrate keto group as an initial degradation step in induced cells. It is concluded that the formerly described steroid inducible hydroxysteroid dehydrogenases/carbonyl reductases present in Comamonas testosteroni contribute to these altered phenotypes, thus establishing steroid-inducible catabolic pathways as important defense processes against natural and synthetic toxicants in certain bacteria, which are present in the intestinal microflora of mammalian species as well as in soil samples.