Sulphide-induced energy deficiency in colonic cells is prevented by glucose but not by butyrate.

Sarah Hulin, Sukhdev Singh, MA Chapman, A Allan, Michael Langman, Margaret Eggo

Research output: Contribution to journalArticle

17 Citations (Scopus)


BACKGROUND: In ulcerative colitis, hydrogen sulphide is postulated to impair colonocyte butyrate metabolism, leading to cellular energy deficiency and dysfunction. AIMS: To determine the effects of sulphide exposure on butyrate metabolism and adenosine triphosphate levels of HT29 colonic epithelial cancer cells, and to establish whether energy deficiency can be prevented by increased butyrate concentrations or the presence of glucose. METHODS: HT29 cells were maintained in medium containing 3 mM butyrate, 5 mM glucose, or both substrates. Oxidation rates were measured by 14CO2 release from 14C-labelled substrates. Cellular adenosine triphosphate was assayed using the luciferin/luciferase chemiluminescent method. The effects of sulphide (0-5 mM) on substrate oxidation and adenosine triphosphate levels and of increasing butyrate concentration (0-30 mM) with sulphide were observed. RESULTS: HT29 cells showed similar energy substrate usage to primary colonocyte cultures. Sulphide exposure inhibited butyrate oxidation and led to a reduction in cellular adenosine triphosphate. This fall was prevented by co-incubation with glucose, but not by increasing concentrations of butyrate. CONCLUSIONS: HT29 cells utilize butyrate as an energy substrate and represent a useful in vitro model of the effects of sulphide on colonocytes. Sulphide inhibits butyrate oxidation and leads to demonstrable energy deficiency, prevented by the presence of glucose but not by increased butyrate concentrations.
Original languageEnglish
Pages (from-to)325-31
Number of pages7
JournalAlimentary Pharmacology & Therapeutics
Issue number2
Publication statusPublished - 1 Feb 2002


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