Iron Mineral (Fe) – An overview of iron

Iron mineral or Iron (Fe) is an essential trace element for the body’s hematopoiesis. Iron together with protein forms hemoglobin, transports O2 and CO2, prevents anemia and participates in the components of oxidizing enzymes. Nutritional anemia due to iron deficiency is very common in the world, especially in developing countries. In addition to not providing an adequate source of iron in the diet, factors that affect iron absorption also contribute to iron-deficiency anemia.

1. Function of iron minerals

Iron is a special mineral, with important roles in the body such as:

a. Making heme: Iron in the form of ferrous (Fe2+) binds to 4 pyrrole rings to form the heme nucleus – a component of hemoglobin in red blood cells, needed to transport oxygen around the body and in the form of myoglobin, for storage and use of oxygen in the body. Oxygen is released in tissues from hemoglobin used in oxidative metabolism. Hemoglobin binds to carbon dioxide in tissues and carries CO2 to the lungs for removal from the body.

b. Generating energy, synthesizing DNA: Iron participates in redox reactions as a reversible electron that allows iron to go back and forth between 2 reduced iron forms (Fe 2+) and oxidized iron forms (Fe 3+ ) . Iron is present as a component of the enzyme responsible for electron transport and energy generation in mitochondrial respiration, the citric acid cycle, for ribonucleotide reductase, which is essential for DNA synthesis. These enzymes can be divided into heme iron enzymes (cytochromes, peroxidase, catalase, DcytB, etc.), non-heme iron enzymes (iron-sulfur complex, ribonucleotide reductase).

c. In immune function: Evidence suggests that iron is fundamental for the normal development of the immune system. Its deficiency affects the ability of an adequate immune response. The role of iron in immunity is required for the proliferation and maturation of immune cells, especially lymphocytes, involved in inducing a specific response to infection.

2. Iron minerals – What will be the symptoms when the body is deficient? 

Nutritional anemia due to iron deficiency is very common in the world, especially in developing countries. Iron deficiency leads to anemia and symptoms of iron deficiency anemia are:

– Fatigue, dizziness, headache

– Blue skin, pale mucous membranes, pale tongue

– Chest pain, difficulty breathing

– Sensitive to temperature, cold hands and feet

– Difficulty concentrating, heart palpitations

3. How are iron minerals absorbed?

a. Absorption site of iron minerals

Iron uptake and transport depends on specific cellular transport mechanisms. The body’s iron requirement is the main physiological factor and mainly determines the amount of iron absorbed. Absorption occurs mainly in the duodenum and the first part of the small intestine, where a low pH favors iron absorption.

Iron-absorbing carrier proteins are located on the apical surfaces of intestinal mucosal cells in contact with the intestinal lumen and nutrients, which are then either retained by intestinal mucosal cells or transported to the basement membrane and bound to the serum transferrin. A variety of organic molecules have specific roles in binding free iron, carrying iron in the circulation and delivery to functional sites or, if not immediately required, depositing iron in a safe form in ferritin, the storage form of iron.

b. Mechanism of transporting iron minerals into the blood

Iron is found in foods as heme or non-heme iron. Heme iron is found almost exclusively in foods of animal origin such as hemoglobin and myoglobin. Non-heme iron is found in animal and plant tissues, fortified foods, and supplements.

These two forms of iron are absorbed by separate mechanisms. The divalent metal transporter 1 (DMT1) transports inorganic and Fe2+-specific iron across the brush border into intestinal mucosal cells. Duodenal cytochrome B reductase (DcytB) converts dietary iron to a more soluble iron state.

In enterocytes, iron 2 enters a labile or “exchangeable” iron group, from where it can enter three different pathways, depending on the body’s requirements: local delivery to mitochondria for heme synthesis; condensing into the iron depot ferritin (and emptying into the intestinal lumen at the end of the intestinal cell life cycle); or transferred to the basic transporter (ferroportin 1) for translocation into the body.

The mechanism of heme iron absorption remains unclear. However, once inside the enterocytes, the heme molecule is degraded by heme oxygenase to release iron, which then enters the enterocyte exchange zone.

c. Regulation of iron absorption

The absorption of iron from the gastrointestinal tract is dependent on the systemic iron requirement and is regulated by hepcidin. Hepcidin reduces iron absorption by regulating iron absorption in the small intestine, transporting iron across the placenta, and limiting iron release from macrophages and hepatocytes. Hepcidin production in the liver is increased when iron stores are adequate or high and during inflammation.

The mechanism of action of hepcidin may be cell-specific. In macrophages during inflammation, hepcidin prevents iron from leaving the cell by binding to and degrading ferroportin on the cell membrane. In enterocytes, hepcidin downregulates iron absorption by inhibiting DMT1 transcription.

When systemic iron requirements are increased or ferritin iron stores are low, or both, hepcidin production is reduced. The production of hepcidin is also reduced by systemic hypoxia, which stimulates the production of erythropoietin which causes the synthesis of new red blood cells.

References:

[1] C. Geissler and M. Singh, “Iron, Meat and Health”, Nutrients, vol 3, p.h 3, p. 283–316, February 2011, doi: 10.3390/nu3030283.

[2] A. Soyano and M. Gómez, “[Role of iron in immunity and its relation with infections]”, Arch Latinoam Nutr, vol 49, p.h 3 Suppl 2, pp. 40S-46S, September 1999.

Article source: Nutrition Research and Development Institute (https://inrd.vn/)

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