Oral iron intake compromises the integrity of the gastric mucosa and impairs gastrointestinal intestinal motility
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Keywords

Mi c ro nu t r i e n t , or a l i ro n, gastrointestinal tract, stomach, intestinal motility, oxidative stress, iron-overload

Abstract

Background: Iron is an  essential nutrient for health and well-being. Mild gastric discomfort has however been reported following supplemental iron intake.  This  study  was  therefore  designed  to investigate the effects of chronic iron intake on gastric mucosal integrity and motility in male Wistar rats. Methods: Forty  animals  (190-210g)  were randomly divided into 2 equal groups and treated orally with either normal saline (0.2ml/day) or iron (3mg/ kg/day) for 28 days respectively. Thereafter, gastric acid  secretion,  acidity,  ulcer  score,  emptying  and intestinal transit was evaluated. Retro-orbital blood samples  were  also  collected  for  haematological (RBC  count,  PCV,  haemoglobin,  platelets, total  and differential  WBC  counts)  analysis,  serum  iron, transferrin,  ferritin,  and  total  iron-binding  capacity (TIBC).  Stomach  samples  were  also  harvested  for histology,  mucus  and  parietal  cell  counts,  gastric antioxidant  status  (reduced  glutathione,  superoxide dismutase  (SOD),  catalase,  nitric  oxide, malondialdehyde), mucin concentration and total protein. Results: The  iron  treated  animals  showed increased (P<0.05) monocytes, serum iron, ferritin, transferrin, total iron-binding capacity (TIBC), gastric juice pH, malondialdehyde and SOD compared to control. Iron treated group also exhibited increased gastric  nitric  oxide,  mucus  content,  parietal  and mucous cell counts compared to control. Reductions (P<0.05) in gastric catalase, reduced glutathione, gastric emptying and intestinal motility which was accompanied
by gastric mucous cell hyperplasia, coagulation necrosis, and moderate atrophy of parietal and chief cells were also observed in the iron treated group.
Co nc l u s i o n :  Ch r o n i c  i r o n i nt a ke  i mp a i r s gastrointestinal motility, induces gastric oxidative stress, and causes gastric structurally aberrations that may predispose to increased acidity of gastric juice and ulceration.

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