Title: Iron Uptake And Distribution In The Body.

Key words: iron absorption, iron uptake, iron stores, iron deficiency

Date: Oct 1998

Category: 3. Micronutrients

Type: Article

Author: Dr van Rhijn

 

Iron Uptake And Distribution In The Body.

Introduction

Iron deficiency is viewed as a common nutrient deficiency world-wide, and it is important to understand the mechanisms regarding absorption, transport and storage of this vital element.

Iron Absorption

Dietary iron exists in two forms:

On average, only 15% of iron is absorbed from a mixed diet. Iron from blood corpuscles is efficiently re-utilised and the amount of iron in the body is almost entirely controlled by the amount of absorption. Absorption increases when the bodys stores are depleted and when there is a greater demand, as in children and women of childbearing age.

Bioavailability

Various factors and mechanisms affect the bioavailability of Fe.

Absorption is favoured by an acidic environment (stomach acid, food acids and ascorbic acid) as this reduces iron from the ferric to the ferrous form. Absorption is also increased by erythropoietic activity, for example, due to bleeding, haemolysis, high altitude, fructose and alcohol.

Numerous food products inhibit the absorption of iron through various mechanisms. Phosphates and phytates (grains) form insoluble complexes with iron and prevent absorption, as well as tannins (tea), polyphenols (coffee, pulses & nuts), phosphoproteins and albumins (eggs). Trace elements, such as zinc, copper and manganese, may also interfere with iron absorption, due to competition for shared absorptive pathways. Calcium-rich products (milk) have similar inhibitory effects, although the body seems to compensate for this by an increased efficiency of iron absorption. Surgery (partial or total gastrectomy) results in an alkaline milieu that is inhibitory.

Iron Transport

Iron enters the mucosal cells by carrier-mediated passive diffusion and is accumulated in the cells by binding to a protein ferritin. Iron is transported in the blood bound to transferrin (each molecule of transferrin binds 2 Fe2+ ions) to the storage sites for production of haemoglobin (bone marrow), myoglobin (muscle) and cytochrome enzymes (liver). The capacity of ferritin and transferrin to bind with iron is limited, and controls the overall intake of iron.

Iron storage

The total body iron content is about 3-5 g, of which approximately 65% is found in haemoglobin. The rest is stored as haemosiderin (10%), and as ferritin (20%), a protein-iron complex where the protein part, apoferritin, is capable of binding about 4300 Fe3+ ions in its hollow protein shell of 22 subunits. The main storage sites are the reticuloendothelial cells (bone marrow, spleen), hepatocytes (liver) and muscle cells (myoglobin 4%). These cells have transferrin receptors enabling iron to be taken up by receptor-mediated endocytosis.

Iron overload (Inherited or Idiopathic) leads to iron deposition (as insoluble haemosiderin) in the tissues, which may lead to iron-catalysed free radical (hydroxyl) formation and subsequent cell damage. Because of its toxicity in the free state in living cells, most iron is present as complexes within the body.

Conclusion

Knowledge and understanding of the biochemical properties of iron is essential in clinical practice. This will promote proper advice regarding optimal conditions for oral supplementation, considering the fact that it is one of the most commonly prescribed elements in medical practice.