The production of early-labeled bilirubin and erythrocyte hemoglobin heme was measured in rats with iron deficiency anemia, using glycine-2-14C as precursor. The erythropoietic component of the early pigment fraction was significantly augmented and the formation of labeled hemoglobin depressed in the anemic animals, findings characteristic of ineffective erythropoiesis. By contrast, the hepatic component of early-labeled bilirubin was substantially enlarged during the acute response to iron therapy. These experiments illustrate that overproduction of bilirubin may originate from both erythropoietic and hepatic sources of the early-labeled fraction of bile pigment, as well as from hemolysis of circulating red blood cells.

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