Submitted to: Nutrition Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 4, 2007
Publication Date: May 1, 2007
Repository URL: http://handle.nal.usda.gov/10113/46392
Citation: Reeves, P.G., Demars, L.C. 2007. Bovine hemoglobin as the sole source of dietary iron does not support adequate iron status in copper-adequate or copper-deficient rats. Nutrition Research. 27:289-294. Interpretive Summary: Up to 10 percent of the iron consumed in the diets of humans comes from heme and hemoglobin, which are major components in blood. Heme and hemoglobin in our diets come mainly from meats and other animal products, but some heme iron also comes from plants. Humans seem to be able to absorb heme or hemoglobin iron, but some animals cannot. However, these animals are still used from time to time as experimental models to study the absorption of iron from these sources. This experiment was designed to determine whether hemoglobin as the sole source of dietary iron could maintain normal iron levels in growing rats. Because adequate copper levels are required for efficient Fe absorption in the rat, we also determined the effects of copper deficiency on iron levels of rats fed iron as hemoglobin and compared the results with that when rats were fed a salt of iron, ferrous sulfate. The results showed that copper deficiency itself reduced the iron levels in the body regardless of the source of iron. In addition, feeding hemoglobin as the sole source of iron could not maintain normal levels of body iron and caused anemia. Feeding iron as ferrous sulfate did not cause anemia. The results confirm that the rat is not a good experimental model to study the utilization of iron from hemoglobin or heme, and that copper is essential for the utilization of both heme and non-heme iron.
Technical Abstract: This experiment was designed to determine whether hemoglobin as the sole source of dietary iron (Fe) could sustain normal Fe status in growing rats. Because adequate copper (Cu) status is required for efficient Fe absorption in the rat, we also determined the effects of Cu deficiency on Fe status of rats fed Fe as hemoglobin. Forty-eight weanling rats were divided into two groups of 24 rats each. One group was fed a diet containing 5.0 mg Cu/kg (CuA) and the other was fed a diet containing <0.5 mg Cu/kg (CuD). Each of these groups was divided into three sub-groups of eight rats each, fed diets containing 35 mg Fe/kg as ferrous sulfate, 35 mg Fe/kg as bovine hemoglobin, or 70 mg Fe/kg as bovine hemoglobin. After four weeks of consuming the diets, rats were killed and Cu and Fe status assessed. Anemia was present in rats fed CuD diets compared to those fed CuA diets. Anemia was also present in rats fed hemoglobin equal to 35 mg Fe/kg but not when fed hemoglobin equal to 70 mg Fe/kg. Copper concentrations were significantly (P<0.001) lower in the mucosa, serum, liver, and spleen, and kidney of CuD rats compared with that in CuA rats regardless of the dietary Fe source. Iron concentration was significantly (P<0.001) elevated in mucosa and liver, but it was lower in serum (P<0.001) and kidney (P<0.040) of CuD rats, compared with that in CuA rats. Cu deficiency had no effect on spleen Fe concentration. Feeding Fe as hemoglobin at 35 mg/kg produced lower (P<0.001) Fe concentrations in serum and spleen compared with feeding Fe as ferrous sulfate; however, feeding hemoglobin at 70 mg Fe/kg brought these parameters back to normal. Regardless of the dietary Fe concentration as hemoglobin, Fe concentrations in the intestinal mucosa, liver, and kidney were significantly lower than in rats fed ferrous sulfate as the Fe source. Heme oxygenase protein was significantly (P<0.001) higher in rats fed heme Fe than in those fed ferrous sulfate, but was not affected by CuD. This investigation demonstrates that adequate Fe status cannot be maintained in the growing rat with hemoglobin as the sole source of dietary Fe.