Rhodanese, but not cystathionine-γ-lyase, is associated with dextran sulfate sodium-evoked colitis in mice: A sign of impaired colonic sulfide detoxification?

Antecedent hydrogen sulfide elicits an anti-inflammatory phenotype in postischemic murine small intestine: role of heme oxygenase-1

“…However, this explanation is highly unlikely because of the inherent instability of H 2 S in our experimental conditions owing to oxidation in mitochondria, methylation in the cytosol, and scavenging by metalloproteins, disulfide-containing proteins, and heme compounds (10). In addition, H 2 S is subject to rapid catabolism via thiol S-methyltransferase and rhodanese, both of which are expressed in the small intestine (29). Indeed, Doeller et al (6) have designed a polaragraphic H 2 S probe, which is highly sensitive and specific for H 2 S. Using this probe, they are able to eloquently show that H 2 S exists in a dynamic steady state in mammalian cells.…”

Hydrogen Sulfide Signaling in the Gastrointestinal Tract

“…Increased sulfide levels are also observed in the trinitrobenzene sulfonic acid-induced murine colitis (115). Perhaps increased sulfide levels are due to reduced levels of rhodanese, or thiol methyltransferase, which is involved in H 2 S detoxification that has been demonstrated in human ulcerative colitis (75,92) and dextran sodium sulfate induced colitis in mice (108). In addition, some investigators have suggested that widely used animal models of ulcerative colitis, with similar features of epithelial damage to ulcerative colitis, are due to increased availability of indigestible sulfate as a substrate for SRB (10).…”

On the dynamics of nitrite, nitrate and other biomarkers of nitric oxide production in inflammatory bowel disease

“…10 The formation of hydrogen sulphide (H 2 S), produced in the gut by commensal sulfate-reducing bacteria or in tissues by mammalian enzymatic processes, has been suspected to be involved in the etiology of IBD, possibly as a result of impaired detoxification. 73 Of note, H 2 S formation is markedly upregulated in inflammation and known to affect NO availability. 74 It is possible, therefore, that this cross-talk between mediators of inflammatory and hypoxic processes is sufficient to explain the fluctuations in nitrite observed in the present study, and tissue NO metabolite profiling an informative tool to study this cross-talk in vivo.…”