Selenium (Se) is known as an antioxidant mineral and heme iron is a major source for iron intake which can promote carcinogenesis in the body. This study was to investigate the effect of Se on heme-aggravated colon carcinogenesis in mice. Three experimental groups included control [normal diet + AOM (10 mg/kg body weight in saline)/DSS (2% in the drinking water)], [AOM/DSS + hemin (534 mg/kg body weight in CMC)], and [AOM/DSS + hemin + Se (2.82 mg/kg diet in CMC)] groups. Colonic mucosa were stained with 0.3% methylene blue and the colonic polyps, aberrant crypt (AC) and aberrant crypt foci (ACF) were counted. Lipid peroxidation in liver was evaluated by the thiobarbituric acid-reactive substances (TBARS) assay. The number of polyps in the hemin + Se group was 31.6% lower than that in the control group, and 41.4% lower than that in the hemin group. The number of AC in the hemin + Se group was 42.8% lower than that in the control group, and 49.1% lower than that in the hemin group. The number of ACF in the hemin + Se group was 49.0% lower than that in the control group, 45.7% than that in the hemin group. Hepatic TBARS level in the hemin + Se group was significantly low compared with the control group or the hemin group (p<0.05). These findings suggest that Se treatment may be protective against colon carcinogenesis promoted by a high heme-containing diet.