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Cited by 169Inflammatory Bowel DiseaseIron Metabolism and DisordersAntioxidant Activity and Oxidative Stress

Effect of oral iron supplementation on oxidative stress and colonic inflammation in rats with induced colitis

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Carrier, J., Aghdassi, E., Platt, I., Cullen, J., Allard, J. P.·2001·Alimentary Pharmacology & Therapeutics
DOI 10.1046/j.1365-2036.2001.01113.x
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Abstract

BACKGROUND: Iron supplementation may increase disease activity in ulcerative colitis, possibly through the production of reactive oxygen species from the Fenton reaction. AIM: 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.

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  • In subjects with a genetic predisposition, a shift of the microbiome towards colitogenic taxa by iron and disturbance of immune tolerance mechanisms may contribute to the manifestation of inflammatory bowel disease such as Crohn's disease and ulcerative colitis.

    “In subjects with a genetic predisposition both, a shift of the microbiome towards colitogenic taxa by iron and the disturbance of immune tolerance mechanisms, may contribute to the manifestation of inflammatory bowel disease such as Crohn's disease and ulcerative colitis (Carrier et al., 2001(Carrier et al., , 2006;;Chua et al., 2013).”

    From Iron in infection and immunity (2020) · cites this paper as Carrier et al., 2001

    The Discussion reports that oral iron increased disease activity in rats with DSS-induced colitis, supporting a limited link between iron and worsened colonic inflammation. It does not show that iron shifts the microbiome toward colitogenic taxa, disturbs immune tolerance, or contributes to the onset of Crohn’s disease or ulcerative colitis in genetically predisposed people; the Discussion says iron alone did not produce intestinal inflammation in the rats. (LLM, conf=0.85)

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Research works printed but not linked: 6

  1. Grisham MB, Granger DN. Neutrophil-mediated mucosal in- jury. Dig Dis Sci 1988; 33: 6S±15S.
  2. Onderdonk AB, Bartlett JG. The role of bacteria in experi- mental ulcerative colitis. Am J Clin Nutr 1979; 32: 258±65.
  3. Grant GH, Kachnar JF. The proteins of body ¯uids. In: Tritz NW, ed. Fundamentals of Clinical Chemistry. Philadelphia: Saunders, 1976: 298±376.
  4. Bessey OA, Lowry OH, Brock MJ. Quantitative determination of dehydroascorbic acid in small amounts of white cells and platelets. J Biol Chem 1947; 168: 197±205.
  5. Keshavarzian A, Sedghi S, Kanofsky J, et al. Excessive oxygen metabolites by in¯amed colon: analysis by chemiluminescence probe. Gastroenterology 1992; 103: 177±85.
  6. Caughey WS, Watdins JA. Oxyradical and peroxide formation by hemoglobin and myoglobin. In: Greenwald RA, ed. Handbook of Methods for Oxygen Radical Research. Boca Raton, FL: CRC Press, 1985: 95±104.

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Authors
Carrier, J., Aghdassi, E., Platt, I., Cullen, J., & Allard, J. P.
Affiliations
  • University of Toronto (CA)
  • St Joseph's Health Centre (CA)
Corresponding author
Allard, J. P.
ORCID
Venue
Alimentary Pharmacology & Therapeutics
Publisher
Wiley
Published
2001-12-27
Volume
15
Issue
12
Pages
1989-1999
ISSN
  • 0269-2813 (ISSN-L)
  • 1365-2036
DOI
10.1046/j.1365-2036.2001.01113.x
OpenAlex
W2055562038
Cited by
169
References
47
Citations by year
2026: 1 · 2025: 4 · 2024: 4 · 2023: 10 · 2022: 12 · 2021: 10 · 2020: 8 · 2019: 8 · 2018: 5 · 2017: 6 · 2016: 11 · 2015: 10 · 2014: 10 · 2013: 8 · 2012: 4
FWCI
2.00
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 61 d)
Locations
  • Alimentary Pharmacology & Therapeutics (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Crohn's and Colitis Foundation
  • Crohn's and Colitis Foundation of Canada
  • Medical Research Council
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
  • Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
oral iron supplementation, ulcerative colitis, DSS-induced colitis, oxidative stress, colonic inflammation, lipid peroxidation, Fenton reaction, reactive oxygen species, antioxidant vitamins, glutathione peroxidase, iron bioavailability, dose-dependent effects
MeSH terms
Administration, Oral, Animals, Antioxidants, Ascorbic Acid, Colitis, Disease Models, Animal, Drug Interactions, Glutathione Peroxidase, Inflammation, Intestines, Iron, Male, Mucous Membrane, Vitamin E, Lipid Peroxidation, Dextran Sulfate, Rats, Wistar, Reactive Oxygen Species, Oxidative Stress, Dietary Supplements, Rats, In Vitro Techniques

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