Abstract
The HFE mutation is common and, when homozygous, can lead to a morbid accumulation of body iron and the disease hereditary hemochromatosis. Heterozygotes compose 10-15% of the European-American population, and have evidence of elevated body iron compared to homozygous normal people. Dietary iron content was hypothesized to interact with the HFE genotype to influence oxidative damage in mammary and colon tissue. Two groups of HFE-knockout mice were fed a standard iron diet (300 ppm) or a low iron diet (30 ppm). There was a significantly elevated concentration of malondialdehyde (by HPLC) in mammary (305 pmol/g vs. 166, p =.04) and colon (349 pmol/g vs. 226, p =.02) tissue among those mice on the standard iron diet compared to those on the low iron diet. These results suggest that dietary modification may affect the course of iron overload from HFE mutations.
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