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Dear All,
To configure out what is meant from this question, we have to declare the whole story of iron and its progressive journey in the human body to be stored:
Total body iron content is about2gm for women and6 gm. for men. Approximately80% of functional body iron is found in Hemoglobin; the remainder is in myoglobin (the oxygen – carrying protein of a muscle) and iron – containing enzymes (e.g., catalase and cytochromes).
The iron storage pool, represented by hemosiderin and ferritin – bound iron, contains15% to20% of total body iron.
Stored iron is found in all tissues but particularly in liver, spleen, bone marrow and skeletal muscle.
Because serum ferritin is largely derived from the storage pool of iron, its level is a good indicator of the adequacy of body iron stores.
Staining bone marrow for iron – containing macrophages is another useful and simple method for estimating body Iron content.
The normal daily western diet contains10 –20 mg of iron. Most of this is in the form of heme contained in animal products, with the remainder being inorganic iron in vegetables.
About20% of the heme iron (in contrast to1% to2% of non-heme iron) is absorbable, so the average diet contains sufficient iron to balance fixed daily losses.
Iron is absorbed in the duodenum, where it must pass through the apical and basolateral membranes to traverse the villus erythrocytes.
Dietary heme iron is absorbed through a different mechanism that is not yet understood. Only a proportion of heme iron as well as non-heme iron that enters the cell are delivered rapidly to plasma transferrin by the action of various transporters across each of these2 membranes (the apical and basolateral membranes).
To be absorbed by intestinal cells, iron must be in the ferrous oxidation state and bound to protein. Because Ferric form of iron is the predominant form of iron in foods, it must be first reduced to ferrous form by agents such as vitamin C before it can be absorbed. In the intestinal mucosal cells, ferrous form of iron is bound by Apoferritin, and then oxidized by ceruloplasmin to ferric form of iron bound to ferritin.
From there, iron is absorbed in to the blood by apotransferrin, which becomes transferrin as it binds two ferric ions. In plasma, Transferrin carries and releases iron to the bone marrow, where it is incorporated into hemoglobin of RBCs.
After4 months in circulation, red cells are degraded by the spleen, liver and macrophages, which returns iron the circulation where it is bound and carried by transferrin for reuse.
The remainder is bound to mucosal ferritin within the cell, some to be transported more slowly to the blood and some to be lost within the exfoliation of mucosal cells. When the body is replete with iron, most of the iron that enters the cell is bound to ferritin and is lost by exfoliation; in iron deficiency, or when there is ineffective erythropoiesis, transfer to plasma transferrin is enhanced.
Iron is transported in the plasma by an Iron – binding protein called transferrin. In normal persons, transferrin is about33% saturated with iron, yielding serum iron levels that average120 micro gm/dl in men and100 micro gm/dl in women. Thus, the total iron binding capacity of serum is in the range of300 to350 micro gm.
Ferritin is measured in serum by immunochemical methods, such as IRMA, ELISA and Chemiluminescent techniques. Ferritin is decreased in iron deficiency anemia and increased in iron overload and hemochromatosis. Ferritin is often increased in several other conditions, such as chronic infections, malignancies and viral hepatitis.
Thanks,
Lubna Al-Sharif
Iron is stored on ferritin complexes that are present in all cells, but most common in bone marrow, liver, and spleen. The liver's stores of ferritin are the primary physiologic source of reserve iron in the body. The reserves of iron in adults lower in children and women of child-bearing age, than in men and in the elderly due to iron lost through menstruation, pregnancy or lactation. Iron deficiency first effects the storage iron in the body, and depletion of these stores is thought to be relatively non-symptomatic, although some vague and non-specific symptoms have been associated with it. Since so much iron is required for hemoglobin, iron deficiency anemia is the primary clinical manifestation of iron deficiency. Macrophages of the reticuloendothelial system store iron as part of the process of breaking down and processing hemoglobin from engulfed RBCs.
Iron is also stored as a pigment called hemosiderin which is an ill defined deposit of protein and iron, created by macrophages where excess iron is present, either locally or systemically for example among people with iron overload due to frequent blood cell destruction &transfusions. If the systemic iron overload is corrected, over time it hemosiderin is slowly resorbed by macrophages.
In the Liver
hemoglobin and myoglobin.
Ferritin is the protein which store iron in human body.
FERRITIN / Heme groups are part of hemoglobin / Hb / Protein and Fe+++, a protein found in red blood cells that serves to transport oxygen from the lungs to the tissues. Heme groups are also present in myoglobin to store and diffuse oxygen in muscle cells.