Iron metabolism of mice fed low levels of physiologically bound cadmium in oyster or cadmium chloride.

Three feeding studies were conducted with young mice to compare the toxicity of cadmium (Cd) occurring in oyster tissue to that of cadmium chloride (CdCl2). In the first experiment, 5 or 20 ppm dietary Cd as CdCl2 depressed blood hematocrit and hemoglobin concentrations, which were further depressed by the addition of up to 3% oyster to the diet. In the second experiment, 1.5 or 3.0 ppm dietary Cd as CdCl2 did not influence hematopoiesis after 14 days exposure. The percent of the Cd dose retained in the kidney was inversely related to dosage level, directly related in the liver and femur and unaffected by dosage level in the small intestine. The liver-to-kidney ratio of retained Cd increased markedly with dose. In the last experiment, 0, 1.8 or 3.6 ppm Cd as CdCl2 or 1.8 ppm Cd from oyster was fed to mice for 28 days. Diets containing intrinsic oyster Cd at 1.8 ppm were more effective than diets containing CdCl2 at 3.6 ppm Cd for depressing total serum iron (Fe) and percent transferrin saturation and for enhancing ceruloplasmin activity. Oyster Cd was retained at a much lower rate in all tissues compared to CdCl2. Oyster Cd was preferentially retained in the kidney compared to the liver. Intrinsic oyster Cd may be more potent in altering normal Fe metabolism than CdCl2. Interactions with other dietary constituents in oysters which may also influence Fe metabolism, particularly zinc (Zn) and copper (Cu), are discussed.