A level of dietary iron may play a role in colon carcinogenesis. The effect of dietary iron on colon carcinogenesis was investigated in male ICR mice. Five-week old mice were acclimated for one week and fed on iron-normal diet (35 ppm Fe), iron-deficient diet (3 ppm), or iron-overloaded diet (350 ppm Fe) for 8 weeks. Animals received three (0-2nd weeks after starting experiment) injections of azoxymethane (AOM; 10 mg/kg b.w.) to induce colonic aberrant crypt foci (ACF). There were five experimental groups including normal control without AOM, AOM+iron-normal diet (AOM+NFe), AOM+iron-deficient (AOM+LFe), AOM+ironoverloaded diet (AOM+HFe) groups. The total numbers of ACF and aberrant crypt (AC) were measured in the colonic mucosa after staining with methylene blue. The blood and serum were analyzed with a blood cell differential counter and an automatic serum analyzer. The hepatic iron levels were significantly dependent on the presence of iron in the diets. Iron-deficient diet significantly decreased the several hematological values. The values of glutamic oxaloacetic transaminase (GOT) and glutamic pyruvate transaminase (GPT) were also significantly decreased in iron-overloaded or iron-deficient diet groups, compared with normal iron diet group. Dietary iron-deficiency decreased the numbers of ACF (64.9) and AC (79.8) per colon by 20.6 and 21.8%, respectively, compared with AOM+NFe group (72.4 ACF/colon and 90.3 AC/colon). However, ironoverloaded diet increased ACF (82.9) and AC (96.0) induction by AOM, compared with normal iron diet. These results suggest that dietary iron can affect the colon carcinogenesis in the animal model of mice.