Assessment of Iron's Regulatory Impact on Cadmium Bioavailability in Rice-Based Diets Using a Mouse Model.

The r ole of iron (Fe) in regulating cadmium (Cd) relative bioavailability (Cd-RBA) in dietary rice is unclear, limiting our understanding of health risks from dietary rice consumption, particularly for vulnerable groups like women of reproductive age. Given the health threats from long-term low-dose Cd exposure, this knowledge gap is especially concerning. It is thus important to systematically examine how Cd concentration in dietary rice affects Cd-RBA and to assess the regulatory impact of Fe on Cd-RBA. A mouse experiment was conducted using rice feed with four Cd levels and five Fe levels, and the Cd concentrations in the faces, blood, and urine were determined. Fe addition to rice feed inversely correlated with Cd concentrations in mouse organs. Increasing Fe from 150 to 200 mg/kg significantly reduced Cd concentrations (p < 0.05) and lowered Cd relative bioavailability (RBA). Cd excretion through feces mirrored organ accumulation. Blood Cd levels were very low and inversely proportional to Fe concentration (R² = 0.71-0.97). Cd-RBA negatively correlated with Cd level in rice (R² = 0.38-0.96). Liver and kidney had similar Cd-RBA values, but kidneys were more sensitive to low-dose Cd, needing further study on the mechanisms. At 150 to 200 mg/kg Fe, some organs still had increased Cd accumulation and Cd-RBA, possibly due to Cu transport proteins (ATP7A). Urine Cd concentrations remained low and did not correlate linearly with Cd or Fe levels in rice feed, likely due to low Cd levels in experimental rice. It was revealed that there was an overall negative correlation between Cd-RBA and Cd level in rice and confirmed that higher levels of Fe can effectively inhibit the body's absorption of Cd, thereby regulating Cd-RBA in rice. The mechanism is that a high level of Fe inhibits the transport of Cd in intestinal epithelial cells and promotes its efficient excretion from the body with feces. This is confirmed by the corresponding changes in organ Cd enrichment and fecal Cd concentration.