Diminished iron acquisition by cells and tissues of Belgrade laboratory rats.

Iron uptake from transferrin by a variety of cells and tissues of homozygous Belgrade laboratory rats was compared with heterozygotes, and normal and iron-deficient Wistar rats. In all cases the results for homozygous Belgrade rats were lower than for the other animals. The maximal rate of iron uptake by fibroblasts cultured in vitro and iron passage to homozygous fetuses in utero was less than 60% of control values. In vivo studies of 15-day-old Belgrade rats revealed a defect in the homozygotes with reduced iron transfer to heart, liver, brain, and femurs. In addition, adult Belgrade laboratory rats had impaired intestinal iron absorption compared with the genetically normal animals. It is concluded that the defect in iron metabolism in the Belgrade laboratory rat is a ubiquitous one that affects transport of iron across membranes of many types of cells, resulting in low intracellular iron levels. This suggests that the genetic defect leads to a widely expressed abnormality in the structure and/or function of a membrane carrier for iron.