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Abstract
Hepatocyte iron release was studied in vivo in rats. After the injection of iron 59-labeled
ferritin, hemoglobin, or human asialotransferrin, the proportions of the radioactive
iron returned to the plasma and incorporated into stores were determined under various
conditions. Iron 55-labeled rat transferrin was injected at the same time as the 59Fe-labeled compound, and storage iron release was calculated from the cumulative incorporation
of the two isotopes in the red cell mass over 2 weeks. The various 59Fe-labeled compounds were processed differently by the hepatocyte, but the radioactive
iron was incorporated in the same iron stores. About 6% of the hepatocyte storage
iron was released daily in normal rats, but a pool of iron that is not mobilized spontaneously
was clearly identified in iron overload. Iron turnover in the hepatocyte was regulated
by the rate of erythropolesls and fron status of the animal, and inflammation blocked
hepatocyte iron release. A strong correlation between hepatocyte iron release and
plasma transferrin receptor levels was observed (p< 0.001), suggesting that plasma transferrin receptors could mediate the regulation
of hepatocyte iron mobilization in rats.
Abbreviations:
DFO = deferoxamine (), ER = early release (), HEPES = n-2-hydroxyethylpiperazine-n′-2 ethanesulfonic acid (), LR = late release (), PIT = plasma iron turnover (), t12 = half-life ()To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
November 18,
1988
Received in revised form:
November 11,
1988
Received:
July 27,
1988
Footnotes
☆Supported in part by National Institutes of Health Grant HL06242 and by Institut Interuniversitaire des Sciences Nucleaires (Belgium) Grant 4450865.
Identification
Copyright
© 1989 Published by Elsevier Inc.
