Model of reticuloendothelial iron metabolism in humans: Abnormal behavior in idiopathic hemochromatosis and in inflammation

Journal Article · Tue Aug 01 04:00:00 EDT 1989 · Blood; (USA)

OSTI ID:5606070

Fillet, G; Beguin, Y; Baldelli, L ^[1]

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1. Univ. of Liege (Belgium)

Iron transport in the reticuloendothelial (RE) system plays a central role in iron metabolism, but its regulation has not been characterized physiologically in vivo in humans. In particular, why serum iron is elevated and RE cells are much less iron-loaded than parenchymal cells in idiopathic hemochromatosis is not known. The processing of erythrocyte iron by the RE system was studied after intravenous (IV) injection of 59Fe heat-damaged RBCs (HDRBCs) and 55Fe transferrin in normal subjects and in patients with iron deficiency, idiopathic hemochromatosis, inflammation, marrow aplasia, or hyperplastic erythropoiesis. Early release of 59Fe by the RE system was calculated from the plasma iron turnover and the 59Fe plasma reappearance curve. Late release was calculated from the ratio of 59Fe/55Fe RBC utilization in 2 weeks. The partitioning of iron between the early (release from heme catabolism) and late (release from RE stores) phases depended on the size of RE iron stores, as illustrated by the inverse relationship observed between early release and plasma ferritin (P less than .001). There was a strong correlation between early release and the rate of change of serum iron levels during the first three hours in normal subjects (r = .85, P less than .001). Inflammation produced a blockade of the early release phase, whereas in idiopathic hemochromatosis early release was considerably increased as compared with subjects with similar iron stores. Based on these results, we describe a model of RE iron metabolism in humans. We conclude that the RE system appears to determine the diurnal fluctuations in serum iron levels through variations in the immediate output of heme iron. In idiopathic hemochromatosis, a defect of the RE cell in withholding iron freed from hemoglobin could be responsible for the high serum iron levels and low RE iron stores.

• OSTI ID: 5606070
• Journal Information: Blood; (USA), Journal Name: Blood; (USA) Vol. 74:2; ISSN BLOOA; ISSN 0006-4971
• Country of Publication: United States
• Language: English

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59 BASIC BIOLOGICAL SCIENCES
ANIMAL TISSUES
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
BIOLOGICAL MATERIALS
BLOOD
BLOOD CELLS
BLOOD FORMATION
BLOOD PLASMA
BODY
BODY FLUIDS
DAYS LIVING RADIOISOTOPES
DISEASES
ELECTRON CAPTURE RADIOISOTOPES
ELEMENTS
ENERGY
ERYTHROCYTES
ERYTHROPOIESIS
EVEN-ODD NUCLEI
GLOBULINS
GLOBULINS-BETA
HEAT
HEMIC DISEASES
INFLAMMATION
INTERMEDIATE MASS NUCLEI
IRON
IRON 55
IRON 59
IRON ISOTOPES
ISOTOPE APPLICATIONS
ISOTOPES
MATERIALS
MEMBRANE TRANSPORT
METABOLISM
METALLOPROTEINS
METALS
NUCLEI
ORGANIC COMPOUNDS
PATHOGENESIS
PATHOLOGICAL CHANGES
PATIENTS
PROTEINS
RADIOISOTOPES
RETICULOENDOTHELIAL SYSTEM
SYMPTOMS
TISSUES
TRACER TECHNIQUES
TRANSFERRIN
TRANSITION ELEMENTS
YEARS LIVING RADIOISOTOPES