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Iron supplementation modulates genes involved in oxidoreductase activity, including prostaglandin‐endoperoxide synthase 2 in intestinal tumors
Author(s) -
Swain James,
Li Chunbiao,
Leahy Patrick
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.692.4
Subject(s) - oxidoreductase , microbiology and biotechnology , gene , biology , biochemistry , chemistry , enzyme
To determine the effect of excess dietary iron on gene expression of intestinal tumors in an animal model of human familial adenomatous polyposis, male C57BL/6J Apc Min/+ mice were fed adequate and excess amounts of iron (ferrous sulfate: 45 vs. 450 mg iron/kg AIN‐93M[M] diet). After 10 wk, mice were sacrificed and intestines removed. Tumors and adjacent non‐tumor tissue were excised and RNA isolated for micro‐array analysis (n=3/group; Mouse Genome 430A 2.0 arrays; Affymetrix) and RT‐PCR. Pathway mapping was performed to reveal gene networks (Pathway Studio 4.0, Ariadne Genomics, Inc.; Gene Spring , Agilent, Inc.; Searcher, Lucidyx). Bayesian ANOVA was used for micro‐arrays. Data show that intestinal tumors alter expression of a group of genes involved in oxidoreductase activity when exposed to excess iron. Differentially expressed genes include prostaglandin‐endoperoxide synthase 2, retinol saturase, alcohol dehydrogenase, deiodinase, cytochrome P450 (family 2, 4), and glutathione peroxidase. Findings reveal that iron supplementation modulates oxidoreductase activity of intestinal tumors, possibly in response to the pro‐oxidative, pro‐inflammatory effects of excess intraluminal iron. Supported in part by grants IRG‐91‐022 from ACS (to JS) and P30CA43703 from NIH. Ferrous sulfate provided by Crown Technologies, Inc.