title: Dietary iron affects inflammatory status in a rat model of colitis.
abstract: Iron deficiency anemia is a common feature in inflammatory bowel disease, and oral supplementation is one of the mainstay therapies. However, there is some concern that oral iron supplementation may lead to oxidative stress and exacerbation of inflammation. Our objective was to study the effect of severely deficient, moderately deficient, normal and high iron status on oxidative stress and the course of inflammation in a rat model of colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). The rats were randomly assigned to receive the low-iron diet for 3 (moderately iron-deficient group, n = 16) or 5 (severely iron-deficient group, n = 16) wk, the normal iron diet for 2 wk (normal iron group, n = 16) or the high-iron diet for 2 wk (high-iron group, n = 16). Malondialdehyde concentration, electroparamagnetic resonance measurement, myeloperoxidase activity, and histological analysis were used to evaluate oxidative stress. Noncolitic rats in the high-iron group had higher oxidative stress parameters than those in the other groups. The induction of colitis resulted in severe inflammatory changes in the high-iron and severely iron-deficient groups, and produced higher histological scores in the colon of the normal and high-iron groups. Iron overload, oxidative stress, and inflammation were lower in the moderately iron-deficient group compared with the other 3 groups. In conclusion, we suggest that low rather than normal or high iron supplementation should be considered for the treatment of iron deficiency in inflammatory bowel disease.
authors.affiliation: School of Nutritional Sciences, The Hebrew University of Jerusalem, Rehovot, Israel.
authors.forename: Ram
authors.initials: R
authors.lastname: Uritski
authors.forename: Iris
authors.initials: I
authors.lastname: Barshack
authors.forename: Itzhak
authors.initials: I
authors.lastname: Bilkis
authors.forename: Kebreab
authors.initials: K
authors.lastname: Ghebremeskel
authors.forename: Ram
authors.initials: R
authors.lastname: Reifen
mesh_terms: D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology*; D003106:Colon / Q000378:metabolism / Q000473:pathology; D004305:Dose-Response Relationship, Drug; D005293:Ferritins / Q000097:blood; D007501:Iron / Q000097:blood / Q000378:metabolism; D019266:Iron, Dietary / Q000008:administration & dosage*; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009994:Osmolar Concentration; D018384:Oxidative Stress; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013438:Sulfhydryl Compounds / Q000378:metabolism; D014302:Trinitrobenzenesulfonic Acid
chemical_list: D019266:Iron, Dietary; D013438:Sulfhydryl Compounds; D008315:Malondialdehyde; D014302:Trinitrobenzenesulfonic Acid; D005293:Ferritins; D007501:Iron; D009195:Peroxidase