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Thiolmethyltransferase activity in the human colonic mucosa: Implications for ulcerative colitis

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dc.contributor.authorMoore, J.
dc.contributor.authorBabidge, W.
dc.contributor.authorMillard, S.
dc.contributor.authorRoediger, W.
dc.date.issued1997
dc.description.abstractUlcerative colitis is associated with a selective reduction of n-butyrate oxidation by the colonic epithelial cells although the reason for this has been unclear. Colonic epithelial cell n-butyrate oxidation can be inhibited in vitro by incubation with sulphide but the role of mucosal detoxification of sulphide in the metabolic welfare of the colonic mucosa has not been examined. This study aimed to assess the role mucosal detoxification of sulphide by thiolmethyltransferase (TMT)-mediated methylation may play in protecting the healthy colonic mucosa from the adverse effects of luminal sulphide. Colonic epithelial cell suspensions from healthy human proximal (n = 9) and distal colon (n = 10) were incubated in the presence of 14C-labelled n-butyrate (5 mmol/L) alone, butyrate plus sodium hydrogen sulphide (NaHS) (1.5 mmol/L), or butyrate plus NaHS plus S-adenosyl-methionine 1,4 butane disulphonate (SAMe) (5 mmol/L). Study end points were metabolic performance (14CO2 production) and mucosal TMT activity. Incubation with NaHS induced a significant inhibition of 14CO2 production compared with control incubations (P < 0.001) which was similar for proximal and distal colonic cell suspensions. S-adenosyl-methionine 1,4 butane disulphonate reversed this effect completely in proximal but not in distal cell incubations, suggesting a greater susceptibility of the distal colon to the sulphide effect. Although median whole mucosal TMT values did not differ between proximal and distal colonic mucosa, a non-normal distribution of distal TMT values was observed. However, neither the degree of sulphide inhibition of control 14CO2 production nor the degree to which SAMe reversed this inhibition correlated with whole mucosal TMT activity. The study concluded that regional variation exists in TMT activity in the human colon but whilst methylation appears to protect colonic epithelial cells against sulphide-induced inhibition of n-butyrate oxidation, this cannot be directly correlated with mucosal TMT activity.
dc.description.statementofresponsibilityMoore, James WE; Babidge, Wendy J; Millard, Sue H; Roediger, William EW
dc.identifier.citationJournal of Gastroenterology and Hepatology (Australia), 1997; 12(9-10):678-684
dc.identifier.doi10.1111/j.1440-1746.1997.tb00534.x
dc.identifier.issn0815-9319
dc.identifier.issn1440-1746
dc.identifier.orcidBabidge, W. [0000-0002-7063-7192]
dc.identifier.orcidRoediger, W. [0000-0002-6480-4804]
dc.identifier.urihttp://hdl.handle.net/2440/10187
dc.language.isoen
dc.publisherBLACKWELL SCIENCE
dc.source.urihttps://doi.org/10.1111/j.1440-1746.1997.tb00534.x
dc.subjectIntestinal Mucosa
dc.subjectColon
dc.subjectErythrocyte Membrane
dc.subjectHumans
dc.subjectColitis, Ulcerative
dc.subjectCarbon Dioxide
dc.subjectSulfides
dc.subjectButyric Acid
dc.subjectButyrates
dc.subjectMethyltransferases
dc.subjectS-Adenosylmethionine
dc.subjectAged
dc.subjectFemale
dc.subjectMale
dc.titleThiolmethyltransferase activity in the human colonic mucosa: Implications for ulcerative colitis
dc.typeJournal article
pubs.publication-statusPublished

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