Bismuth(III) interactions with Desulfovibrio desulfuricans: inhibition of cell energetics and nanocrystal formation of Bi2S3 and Bi0.

Sulfate-reducing bacteria have been suggested to have an etiological role in the development of inflammatory bowel diseases and ulcerative colitis in humans. Traditionally. bismuth compounds have been administered to alleviate gastrointestinal discomfort and disease symptoms. One mechanism by which this treatment occurs is through binding bacterial derived hydrogen sulfide in the intestines. With the addition of bismuth-deferiprone, bismuth-citrate and bismuth subsalicylate to reactions containing cells of D. desulfuricans ATCC 27774, the oxidation of H2 with sulfate as the electron acceptor was inhibited but H2 oxidation with nitrate, nitrite and sulfite was not reduced. Our research suggests that a target for bismuth inhibition of D. desulfuricans is the F1 subunit of the ATP synthase and, thus, dissimilatory sulfate reduction does not occur. At sublethal concentrations, bismuth as Bi(III) is precipitated by hydrogen sulfide produced from respiratory sulfate reduction by D. desulfuricans. Nanocrystals of bismuth sulfide were determined to be Bi2S3 through the use of high resolution transmission electron microscopy imaging with X-ray energy-dispersive spectroscopy analysis. In the absence of sulfate, D. desulfuricans oxidizes H2 with the reduction of Bi(III) to Bi0 and this was also established by X-ray energy-dispersive spectroscopy analysis.