INRA, AgroParisTech, CRNH IdF, UMR 914 Nutrition Physiology and Ingestive Behavior, Paris, France.
Amino Acids. 2010 Jul;39(2):335-47. doi: 10.1007/s00726-009-0445-2. Epub 2009 Dec 18.
Hydrogen sulfide (H(2)S) is present in the lumen of the human large intestine at millimolar concentrations. However, the concentration of free (unbound) sulfide is in the micromolar range due to a large capacity of fecal components to bind the sulfide. H(2)S can be produced by the intestinal microbiota from alimentary and endogenous sulfur-containing compounds including amino acids. At excessive concentration, H(2)S is known to severely inhibit cytochrome c oxidase, the terminal oxidase of the mitochondrial electron transport chain, and thus mitochondrial oxygen (O(2)) consumption. However, the concept that sulfide is simply a metabolic troublemaker toward colonic epithelial cells has been challenged by the discovery that micromolar concentration of H(2)S is able to increase the cell respiration and to energize mitochondria allowing these cells to detoxify and to recover energy from luminal sulfide. The main product of H(2)S metabolism by the colonic mucosa is thiosulfate. The enzymatic activities involved in sulfide oxidation by the colonic epithelial cells appear to be sulfide quinone oxidoreductase considered as the first and rate-limiting step followed presumably by the action of sulfur dioxygenase and rhodanese. From clinical studies with human volunteers and experimental works with rodents, it appears that H(2)S can exert mostly pro- but also anti-inflammatory effects on the colonic mucosa. From the available data, it is tempting to propose that imbalance between the luminal concentration of free sulfide and the capacity of colonic epithelial cells to metabolize this compound will result in an impairment of the colonic epithelial cell O(2) consumption with consequences on the process of mucosal inflammation. In addition, endogenously produced sulfide is emerging as a prosecretory neuromodulator and as a relaxant agent toward the intestinal contractibility. Lastly, sulfide has been recently described as an agent involved in nociception in the large intestine although, depending on the experimental design, both pro- and anti-nociceptive effects have been reported.
硫化氢 (H(2)S) 以毫摩尔浓度存在于人体大肠腔中。然而，由于粪便成分具有很大的结合硫化物的能力，游离（未结合）的硫化物浓度处于微摩尔范围。H(2)S 可以由肠道微生物群从包括氨基酸在内的饮食和内源性含硫化合物中产生。在浓度过高的情况下，H(2)S 已知会严重抑制细胞色素 c 氧化酶，即线粒体电子传递链的末端氧化酶，从而抑制线粒体氧 (O(2)) 的消耗。然而，当发现微摩尔浓度的 H(2)S 能够增加细胞呼吸并为线粒体提供能量，使这些细胞能够从肠腔硫化物中解毒和回收能量时，硫化物仅仅是结肠上皮细胞的代谢麻烦制造者的概念就受到了挑战。结肠黏膜中 H(2)S 代谢的主要产物是硫代硫酸盐。结肠上皮细胞中硫化物氧化涉及的酶活性似乎是硫化物醌氧化还原酶，被认为是第一步和限速步骤，随后可能是硫双加氧酶和转硫酶的作用。从人类志愿者的临床研究和啮齿动物的实验工作来看，H(2)S 似乎对结肠黏膜主要发挥促炎作用，但也有抗炎作用。根据现有数据，我们可以提出这样的假设：即腔游离硫化物的浓度与结肠上皮细胞代谢这种化合物的能力之间的不平衡将导致结肠上皮细胞 O(2)消耗受损，从而影响黏膜炎症过程。此外，内源性产生的硫化物正在成为一种促分泌的神经调节剂，并作为一种对肠道收缩性的松弛剂。最后，硫化物最近被描述为大肠中参与伤害感受的一种物质，尽管根据实验设计，既报道了促伤害感受作用，也报道了抗伤害感受作用。
