Summary. Over 85% of ferritin 59Fe is recovered in the liver of rats within 24 hr of its intravenous injection. Autoradiographic studies have shown that this hepatic uptake is restricted entirely to the parenchymal cells. Following its hepatocellular uptake ferritin is catabolized and its iron moiety is recombined with locally produced apoferritin. The rate of hepatic uptake is reduced by bleeding and enhanced by inflammation. The electrophoretic properties and hepatic handling of ferritin preparations derived from the liver (parenchymal) or spleen (reticuloendothelial) are identical. These findings suggest that the increased amounts of circulating ferritin found in pathologic conditions such as transfusion haeniosiderosis and ineffective erythropoiesis, might play a significant role in the production of parenchymal iroll overload.
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Unger et al. (1974) studied this question.
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