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|dc.identifier.citation||ANZ Journal of Surgery, 1997; 67(5):245-249||-|
|dc.description.abstract||<h4>Background</h4>Several lines of evidence suggest a possible role for reduced forms of sulphur (including sulphide) in ulcerative colitis. The aims of this study were to assess the metabolic profile of colonic epithelial cells after treatment in vivo with hydrogen sulphide and correlate this with mucosal histological appearances.<h4>Methods</h4>Adult Sprague-Dawley rats had antegrade Roux-en-Y colostomies fashioned to allow access to the 'in-flow' bowel. Animals were treated with 2 mL sodium hydrosulphide (10, 20, 30 mmol/L) or saline control twice daily via the stoma for four (acute experiments) and 90 (chronic experiments) days. Isolated colonic epithelial cell suspensions prepared from such animals were incubated in the presence of [1-14C]-labelled n-butyrate (5 mmol/L) or [6-14C]glucose (5 mmol/L). Metabolic performance was measured radiometrically (14CO2 production) and enzymatically (ketone body production and lactogenesis). The histological appearances of treated mucosa were scored for acute inflammatory changes.<h4>Results</h4>There was a highly significant reduction in 14CO2 production from both n-butyrate and glucose in all groups compared to the control in both acute and chronic experiments. There was no difference between groups with respect to histological appearance and no evidence of acute inflammation in any specimen.<h4>Conclusions</h4>Sodium hydrosulphide impairs rat colonic epithelial metabolic performance in vivo, but does not produce mucosal inflammation.||-|
|dc.title||Hydrogen sulphide produces diminished fatty acid oxidation in the rat coloin in vivo: implications for ulcerative colitis||-|
|dc.identifier.orcid||Babidge, W. [0000-0002-7063-7192]||-|
|dc.identifier.orcid||Roediger, W. [0000-0002-6480-4804]||-|
|Appears in Collections:||Aurora harvest 4|
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