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Iron metabolism in rats with acute turpentine-induced inflammation was evaluated. In acute inflammation, reduced plasma iron and total iron-binding capacity values, shortened plasma iron disappearance time and lower plasma iron turnover were observed. The administration of 59Fe chondroitin ferrous sulfate in order to evaluate the reticuloendothelial (RE) function revealed a significantly increased 59Fe retention in the liver and lower incorporation into red blood cells. Radioactivity in hepatic RE cells was higher in acute inflammation than in control. These results suggest the possibility of a block in the transfer of iron from RE cells to the plasma iron pool during acute inflammation.
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