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.

已经有人提出，硫酸盐还原菌在人类炎症性肠病和溃疡性结肠炎的发生中具有病因学作用。传统上。已施用铋化合物以减轻胃肠不适和疾病症状。发生这种处理的一种机制是通过将细菌衍生的硫化氢结合在肠道中。在含有脱硫尿杆菌ATCC 27774的反应池中添加铋-去铁酮，柠檬酸铋和水杨酸铋时，H ₂被硫酸盐作为电子受体的氧化被抑制，而H ₂被硝酸盐，亚硝酸盐和亚硫酸盐氧化的作用并未被抑制。减少。我们的研究表明，抑制铋的目标是D. desulfuricans是ATP合酶的F ₁亚基，因此不会发生异化硫酸盐还原反应。在亚致死浓度下，铋被Bi（III）沉淀，这是由于脱硫双歧杆菌（D.desulfuricans）通过呼吸作用将硫酸盐还原而产生的硫化氢沉淀出来的。通过使用高分辨率透射电子显微镜成像和X射线能量色散光谱分析，确定了硫化铋的纳米晶体为Bi ₂ S ₃。在不存在硫酸盐的情况下，脱硫尿酸杆菌将H ₂氧化，使Bi（III）还原为Bi ⁰，这也是通过X射线能量色散光谱分析确定的。