title: Effect of oral iron supplementation on oxidative stress and colonic inflammation in rats with induced colitis.
abstract: BACKGROUND
  Iron supplementation may increase disease activity in ulcerative colitis, possibly through the production of reactive oxygen species from the Fenton reaction.
  
  
  OBJECTIVE
  To assess the effects of two doses of oral iron on intestinal inflammation and oxidative stress in experimental colitis.
  
  
  METHODS
  Colitis was induced in rats by giving 5% dextran sulphate sodium in drinking water for 7 days. First, using a 2 x 2 factorial design, rats with or without dextran sulphate sodium received the regular diet or a diet containing iron 3%/kg diet. Second, rats with dextran sulphate sodium-induced colitis were supplemented with iron 0.3%/kg diet and compared with rats on dextran sulphate sodium and regular diet. The body weight change, histological scores, colon length, rectal bleeding, plasma and colonic lipid peroxides, colonic glutathione peroxidase and plasma vitamin E and C were measured. Faecal analysis for haem and total, free and ethylenediaminetetra-acetic acid-chelatable iron was also performed.
  
  
  RESULTS
  Iron 3% and iron 0.3% increased the activity of dextran sulphate sodium-induced colitis, as demonstrated by higher histological scores, heavier rectal bleeding and further shortening of the colon. This was associated with increased lipid peroxidation and decreased antioxidant vitamins. Faecal iron available to the Fenton reaction was increased in a dose-dependent manner.
  
  
  CONCLUSIONS
  Iron supplementation taken orally enhanced the activity of dextran sulphate sodium-induced colitis and is associated with an increase in oxidative stress.
authors.affiliation: Department of Medicine, University of Toronto, Toronto, Ont, Canada.
authors.forename: J
authors.initials: J
authors.lastname: Carrier
authors.forename: E
authors.initials: E
authors.lastname: Aghdassi
authors.forename: I
authors.initials: I
authors.lastname: Platt
authors.forename: J
authors.initials: J
authors.lastname: Cullen
authors.forename: J P
authors.initials: JP
authors.lastname: Allard
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001205:Ascorbic Acid / Q000378:metabolism; D003092:Colitis / Q000139:chemically induced / Q000517:prevention & control*; D016264:Dextran Sulfate / Q000494:pharmacology; D019587:Dietary Supplements; D004195:Disease Models, Animal; D004347:Drug Interactions; D005979:Glutathione Peroxidase / Q000187:drug effects; D066298:In Vitro Techniques; D007249:Inflammation / Q000139:chemically induced / Q000517:prevention & control; D007422:Intestines / Q000187:drug effects; D007501:Iron / Q000097:blood / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009092:Mucous Membrane / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D014810:Vitamin E; D016264:Dextran Sulfate; D007501:Iron; D005979:Glutathione Peroxidase; D001205:Ascorbic Acid