The localization of iron in developing erythrocytes of normal and copper-deficient rats was studied by electron microscopy. Lead treatment, by interfering with heme synthesis, resulted in accumulation of iron in mitochondria and vesicles of the developing erythrocyte in normal animals. In similarly treated copper-deficient rats, iron did not accumulate in the mitochondria although it was concentrated in vesicles. The copper-deficient animal, therefore, seems to have an impaired uptake of iron by the mitochondria where it combines with protoporphyrin to form heme, in addition to the previously recognized defect in the release of iron into the circulation from the intestinal mucosa, reticulo-endothelial system and hepatocyte.

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