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The purpose of this study was to estimate the iron concentration in the liver, spleen and brain of control rats and rats overloaded with iron and to determine the distribution of iron and of transferrin (TF). Iron was administered to Wistar rats by food supplemented with 3% carbonyl iron for 3 months, or intraperitoneally, or intraveneously as iron polymaltose for 4 months (total administered dose: 300 or 350 mg/rat, respectively). Iron concentration was estimated by atomic absorption spectrophotometry and iron- and TF-distribution histochemically and immunohistochemically, respectively. In control rats the organ with the highest iron content was the spleen, followed by the liver and brain. After iron loading the increase of iron in the liver was greater than that of the spleen; iron concentration in the brain did not change significantly. Distribution of iron in the liver was in Kupffer cells throughout the lobule and in hepatocytes at its periphery. No difference in the number of positive cells or staining intensity for TF was observed between control rats and iron overloaded animals in the liver or central nervous system (CNS); the spleen was negative for TF. Distribution of TF in the liver showed a centrilobular localisation in hepatocytes. TF reaction in the brain occurred in oligodendrocytes, vessel walls, choroid plexus epithelial cells and some neurons. In conclusion, experimental iron overload in rats leads to iron uptake mainly by reticuloendothelial (RE) cells and hepatocytes, indicating that hepatocytes are of particular importance for iron metabolism. Iron uptake by the brain was not significant, probably because the brain is protected against iron overload. Iron overload did not influence location and quantity of TF in the liver and CNS, whereas the visualisation of iron and TF did not coincide. This indicates that TF may have other functions beyond iron transport.

Although hemochromatosis and pathological situations due to chronic iron overload have been extensively described, there is little information about the influence of iron on other trace elements in the cell. The aim of this study was to investigate changes in the concentration of zinc, manganese, and copper in the liver, spleen, and brain of rats after iron overload. Iron overload in Wistar rats was achieved by iron-supplemented diet or by intraperitoneal or intravenous injection of polymaltose iron. Iron, zinc, manganese, and copper were determined by atomic absorption spectrophotometry. Iron overload in rats, regardless of the route of its application, resulted in an increase not only of iron but also of zinc and manganese in the liver and the spleen, whereas the content of these metals in the brain did not change. The copper content of the liver, spleen, and brain remained the same after iron overload. The increase of zinc and manganese in the liver and spleen following iron overload was probably a result not only of increased intestinal absorption but also of increased uptake from the cell. This is also supported by the fact that no increase in the zinc and manganese concentrations occurred in the brain since, despite iron overload, the iron content remained constant.