Abstract
LEARNING OUTCOME: To assess the effects of high iron and low vitamin E status on lipid peroxidation and prostaglandin E 2 synthesis in a model of colon cancer In recent years there has been heightened concern that high iron (Fe) status may increase risk of cancer at several sites, including liver and colon. It has been theorized that Fe enhances carcinogenesis by catalyzing free radical production and lipid peroxidation (LPX). Animals with low vitamin E (VE) status may be more susceptible to Fe-enhanced LPX. Also, studies suggest that prostaglandins, which may be altered by Fe and VE status, play a role in colon cancer. The present study examined the effect of Fe and VE status on LPX and prostaglandin E 2 (PGE 2) synthesis in an animal model of colon cancer. In a 2×2×2 factorial design, male Sprague Dawley rats were fed 2 levels of Fe (adequate- 45 mg/kg; high- 450 mg/kg diet), and 2 levels of VE (low- 15 IU/kg; adequate- 100 IU/kg diet) for 3 weeks, and then were treated with saline or the carcinogen azoxymethane (AOM; 30 mg/kg; 2 week protocol). The study continued for an additional 6 weeks. Liver and colonic mucosa were collected for analysis at 3 and 10 weeks. Liver Fe, a key indicator of Fe status, was increased 162% and 71% at 3 and 10 weeks, respectively, in rats fed high Fe diets (p=0.0001). LPX of liver was significantly enhanced by high Fe diets after 3 (p<0.02) and 10 (p<0.03) weeks of treatment. Further, there was a trend toward higher liver LPX in rats fed high Fe, low VE diets (p<0.15) compared to other groups. In colonic mucosa, while lipid peroxidation was increased by AOM (p<0.03), and PGE 2 synthesis was decreased by AOM (p<0.02), neither Fe nor VE status had any effect on these indices. Thus our study suggests that dietary Fe levels 10 times higher than recommended do not alter colon LPX or PGE 2 synthesis in a model of colon carcinogenesis even when VE intake is low. Supported by GA AES #H-757.
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