Impaired Detoxication of Hydrogen Sulfide in Ulcerative Colitis?

  title={Impaired Detoxication of Hydrogen Sulfide in Ulcerative Colitis?},
  author={Rhian Picton and Margaret C. Eggo and M. J. S. Langman and S. Singh},
  journal={Digestive Diseases and Sciences},
Impaired butyrate oxidation and raised counts of sulfate-reducing bacteria in the colon of patients with ulcerative colitis (UC) indicate that the disease may be induced or aggravated by hydrogen sulfide toxicity. We aimed to examine enzymatic removal of H2S in erythrocytes and colonic mucosa from controls and patients with UC and Crohn's disease (CD). Rhodanese (RHOD) and thiol methyltransferase (TMT) activities were measured in rectal mucosa and erythrocytes, and plasma thiocyanate was… 
Decreased mucosal sulfide detoxification is related to an impaired butyrate oxidation in ulcerative colitis
An impaired detoxification mechanism of sulfide at TST protein and RNA level in UC was found andlammation was clearly associated with the observed TST deficiency.
Dietary Factors in Sulfur Metabolism and Pathogenesis of Ulcerative Colitis
The increasing severity of inflammation along the proximal-to-distal axis in UC is due to the dilution of beneficial factors, concentration of toxic factors, and changing detoxification capacity of the host, all of which are intimately linked to the nutrient flow from the diet.
Emerging Roles of Hydrogen Sulfide in Inflammatory and Neoplastic Colonic Diseases
The production and storage of H2S, its biological roles and the emerging importance in physiology and pathology of IBD and CRC are discussed.
Endogenous and exogenous hydrogen sulfide promotes resolution of colitis in rats.
In rats, H(2)S modulates physiological inflammation and contributes to the resolution of colitis.
Emerging role of hydrogen sulfide in colonic physiology and pathophysiology
The evidence relating to H2S as a modulator of colonic function and disease is examined, finding evidence linking H2s to colonic nociception, inflammatory bowel disease (IBD), and colorectal cancer.
Luminal sulfide and large intestine mucosa: friend or foe?
The concept that sulfide is simply a metabolic troublemaker toward colonic epithelial cells has been challenged by the discovery that micromolar concentration of H2S is able to increase the cell respiration and to energize mitochondria allowing these cells to detoxify and to recover energy from luminal sulfide.
Hydrogen sulfide: an endogenous mediator of resolution of inflammation and injury.
Results from animal studies suggest that H(2)S-releasing agents are promising therapeutic agents for many indications, but these compounds need to be assessed in a clinical setting.


Sulfur Metabolism in Ulcerative Colitis (Investigation of Detoxification Enzymes in Peripheral Blood)
It is concluded that TMT may be up-regulated in UC to detoxify excess hydrogen sulfide exposed to the peripheral blood compartment from either increased luminal sulfide production or reduced colonic detoxification.
Thiol methyltransferase activity in inflammatory bowel disease
Erythrocyte TMT activity was persistently elevated after proctocolectomy for Crohn's disease and ulcerative colitis and genetic control of T MT activity of erythrocytes in inflammatory bowel disease appear worthwhile.
Mucosal protection against sulphide: importance of the enzyme rhodanese
Rhodanese, located in the submucosa and crypts of the colon, is the principal enzyme involved in H2S detoxication, and TMT does not participate in the detoxication of H 2S.
The contribution of sulphate reducing bacteria and 5-aminosalicylic acid to faecal sulphide in patients with ulcerative colitis
Generation of hydrogen sulphide by sulphate reducing bacteria (SRB) and the effects of 5-aminosalicylic acid (5-ASA) in patients with ulcerative colitis is studied in order to identify a role of this noxious agent in pathogenesis.
Growth and activities of sulphate-reducing bacteria in gut contents of healthy subjects and patients with ulcerative colitis
The findings indicate that the metabolic capabilities of SRB isolated from the human large intestine are not uniform and may respond to the type of substrate available in the gut as well as the rate of passage of digesta.
Pre-illness dietary factors in inflammatory bowel disease.
An association was found between pre-illness diet and subsequent development of UC and CD and the effect of dietary components may be primary or modulatory.
S-methyltransferases in human intestine: differential distribution of the microsomal thiol methyltransferase and cytosolic thiopurine methyltransferase along the human bowel.
Comparison of intestinal with hepatic activities showed that thiopurine methyltransferase is better expressed than thiol methyl transferase in the human intestine, at least with the substrates studied.
Effects of hydrogen sulfide exposure on lung mitochondrial respiratory chain enzymes in rats.
Human erythrocyte thiol methyltransferase: radiochemical microassay and biochemical properties.