title: Free radical production in the esophago-gastro-duodenal mucosa in response to acid and bile.
abstract: Several studies have demonstrated the role of free radicals in causing esophagus-gastro-duodenal mucosal injury. The present study has been designed to investigate: whether acid, bile salts and a combination of bile + acid could determine the production of O2-derived free radicals by oesophageal, gastric and duodenal mucosa; which agent is capable of producing more free radicals and if O2-derived free radicals production depends on the duration of contact with acid, bile salts and their combination. Wistar rats' gastro-intestinal mucosa were perfused with bile, acid and a combination of bile + acid at pH4 and pH2 for 1 hour and 2 hours. Free radical production (FRP) was assessed by chemoluminescence. After 1 hour, the increase in FRP in comparison with control reached statistical significance (P < 0.05) at all tested pH levels in the duodenum, at pH1, 2 and 3 in the esophagus, and at pH1 in the stomach. Comparing different segments, both the esophagus and duodenum behaved similarly, producing more free radicals than the stomach at all pH values. However, this difference reached statistical significance at pH1 and 2 only. In comparison to control, FRP was increased by bile (pH7) infusion after 1 and 2 hours. There was increased FRP in all segments after the infusion of bile at pH2 and 4 in comparison to control. Infusion of bile at pH2 stimulates more FRP than infusion of bile at pH4 in all segments. This increased FRP reaches statistical significance in the esophagus after 2 hours of infusion, in the stomach after 1 and 2 hours of infusion, but in the duodenum it does not reach statistical significance. Acid, bile and bile + acid at pH2 and 4 can cause free radical production in esophageal, gastric and duodenal mucosa. Their role in producing free radicals is different according to the segment and the chemical composition of the solution.
authors.affiliation: Department of Surgical Science, University of Insubria, Varese-Italy. bonil@tin.it
authors.forename: L
authors.initials: L
authors.lastname: Boni
authors.forename: A
authors.initials: A
authors.lastname: Benevento
authors.forename: S M
authors.initials: SM
authors.lastname: Shimi
authors.forename: A
authors.initials: A
authors.lastname: Cuschieri
mesh_terms: D000818:Animals; D001647:Bile Acids and Salts / Q000494:pharmacology*; D004386:Duodenum / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D004947:Esophagus / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005609:Free Radicals / Q000378:metabolism; D005744:Gastric Acid / Q000502:physiology*; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005764:Gastroesophageal Reflux / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008163:Luminescent Measurements; D008297:Male; D009092:Mucous Membrane / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013997:Time Factors; D046509:Tissue Culture Techniques
chemical_list: D001647:Bile Acids and Salts; D005609:Free Radicals; D017382:Reactive Oxygen Species