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Iron (pronounced /ˈаɪɚn/) is a chemical element with the symbol Fe (Latin: ferrum ) and atomic number 26. Iron is a group 8 and period 4 element. Iron and iron alloys (steels) are by far the most common metals and the most common ferromagnetic materials in everyday use. Fresh iron surfaces are lustrous and silvery-grey in color, but oxidise in air to form a red or brown coating of ferrous oxide or rust.

Iron-56 is the second heaviest stable isotope produced by the alpha process in stellar nucleosynthesis, the heaviest being nickel-62; heavier elements require a supernova for their formation. Iron is the most abundant element in the core of red giants, and is the most abundant metal in iron meteorites and in the dense metal cores of planets such as Earth.

Biological role

File:Heme b.png

Structure of Heme b

Main article: Human iron metabolism

Iron is essential to nearly all known organisms. In cells, iron is generally stored in the centre of metalloproteins, because "free" iron (which binds non-specifically to many cellular components) can catalyse production of toxic free radicals. Iron deficiency can lead to iron deficiency anemia.

In animals, iron is often the metal ion incorporated into the heme complex. Heme is an essential component of cytochrome proteins, which mediate redox reactions, and of oxygen carrier proteins such as hemoglobin, myoglobin, and leghemoglobin. Inorganic iron also contributes to redox reactions in the iron-sulfur clusters of many enzymes, such as nitrogenase (involved in the synthesis of ammonia from nitrogen and hydrogen) and hydrogenase. Non-heme iron proteins include the enzymes methane monooxygenase (oxidizes methane to methanol), ribonucleotide reductase (reduces ribose to deoxyribose; DNA biosynthesis), hemerythrins (oxygen transport and fixation in marine invertebrates) and purple acid phosphatase (hydrolysis of phosphate esters).

Iron distribution is heavily regulated in mammals, partly because iron has a high potential for biological toxicity. Iron distribution is also regulated because many bacteria require iron, so restricting its availability to bacteria (generally by sequestering it inside cells) can help to prevent or limit infections. This is probably the reason for the relatively low amounts of iron in mammalian milk. A major component of this regulation is the protein transferrin, which binds iron absorbed from the duodenum and carries it in the blood to cells.[1]

Biological measurement

Iron metabolism

Human iron metabolism is the set of chemical reactions maintaining human homeostasis of iron. The control of this necessary but potentially toxic substance is an important part of many aspects of human health and disease.


Effects of iron deficiency

Human studies

Iron deficiency (sideropenia or hypoferremia) is the most common known form of nutritional deficiency in humans. The direct consequence of iron deficiency is iron deficiency anemia. Groups that are most prone to developing this disease are children and pre-menopausal women.

Animal studies

Iron toxicity

Excessive iron can be toxic, because free ferrous iron reacts with peroxides to produce free radicals, which are highly reactive and can damage DNA, proteins, lipids, and other cellular components. Thus, iron toxicity occurs when there is free iron in the cell, which generally occurs when iron levels exceed the capacity of transferrin to bind the iron.

Iron uptake is tightly regulated by the human body, which has no regulated physiological means of excreting iron. Only small amounts of iron are lost daily due to mucosal and skin epithelial cell sloughing, so control of iron levels is mostly by regulating uptake.[2] However, large amounts of ingested iron can cause excessive levels of iron in the blood because high iron levels can damage the cells of the gastrointestinal tract, preventing them from regulating iron absorption, high blood concentrations of iron damage cells in the heart, liver and elsewhere, which can cause serious problems, including long-term organ damage and even death.

Humans experience iron toxicity above 20 milligrams of iron for every kilogram of mass, and 60 milligrams per kilogram is a lethal dose.[3] Over-consumption of iron, often the result of children eating large quantities of ferrous sulfate tablets intended for adult consumption, is one of the most common toxicological causes of death in children under six.[3] The DRI lists the Tolerable Upper Intake Level (UL) for adults as 45 mg/day. For children under fourteen years old the UL is 40 mg/day.

Regulation of iron uptake is impaired in some people as a result of a genetic defect that maps to the HLA-H gene region on chromosome 6. In these people, excessive iron intake can result in iron overload disorders, such as hemochromatosis. Many people have a genetic susceptibility to iron overload without realizing it or being aware of a family history of the problem. For this reason, it is advised that people do not take iron supplements unless they suffer from iron deficiency and have consulted a doctor. Hemochromatosis is estimated to cause disease in between 0.3 and 0.8% of Caucasians.[4]

The medical management of iron toxicity is complex, and can include use of a specific chelating agent called deferoxamine to bind and expel excess iron from the body.

Human studies

Animal studies

Iron and mental health

Dietary sources

Good sources of dietary iron include red meat, fish, poultry, lentils, beans, leaf vegetables, tofu, chickpeas, black-eyed peas, fortified bread, and fortified breakfast cereals. Iron in low amounts is found in molasses, teff and farina. Iron in meat (haem iron) is more easily absorbed than iron in vegetables,[5] but heme/hemoglobin from red meat has effects which may increase the likelihood of colorectal cancer.[6][7]

Iron provided by dietary supplements is often found as iron (II) fumarate, although iron sulfate is cheaper and is absorbed equally well. Elemental iron, despite being absorbed to a much smaller extent (stomach acid is sufficient to convert some of it to ferrous iron), is often added to foods such as breakfast cereals or "enriched" wheat flour (where it is listed as "reduced iron" in the list of ingredients). Iron is most available to the body when chelated to amino acids - iron in this form is ten to fifteen times more bioavailable[8] than any other, and is also available for use as a common iron supplement. Often the amino acid chosen for this purpose is the cheapest and most common amino acid, glycine, leading to "iron glycinate" supplements.[9] The RDA for iron varies considerably based on age, gender, and source of dietary iron (heme-based iron has higher bioavailability).[10] Infants may require iron supplements if they are breast-fed.[11] Blood donors and pregnant women are at special risk of low iron levels and are often advised to supplement their iron intake.[How to reference and link to summary or text]


See also

References & Bibliography

  1. Tracey A. Rouault. How Mammals Acquire and Distribute Iron Needed for Oxygen-Based Metabolism. URL accessed on 2006-06-19.
  2. Kumar, Vinay, Abbas, Abul K; Fausto, Nelson Anemia. Robbins and Cotran: Pathologic Basis of Disease, 7th edition. Elsevier Saunders. URL accessed on 2008-03-14.
  3. 3.0 3.1 Toxicity, Iron. Emedicine. URL accessed on 2006-06-19.
  4. Durupt S, Durieu I, Nove-Josserand R, et al: [Hereditary hemochromatosis]. Rev Med Interne 2000 Nov; 21(11): 961-71[Medline].
  5. Food Standards Agency - Eat well, be well - Iron deficiency
  6. Sesink AL, Termont DS, Kleibeuker JH, Van der Meer R (1999). Red meat and colon cancer: the cytotoxic and hyperproliferative effects of dietary heme. Cancer Research 59 (22): 5704–9.
  7. Glei M, Klenow S, Sauer J, Wegewitz U, Richter K, Pool-Zobel BL (2006). Hemoglobin and hemin induce DNA damage in human colon tumor cells HT29 clone 19A and in primary human colonocytes. Mutat. Res. 594 (1-2): 162–71.
  8. Pineda O, Ashmead HD (2001). Effectiveness of treatment of iron-deficiency anemia in infants and young children with ferrous bis-glycinate chelate. Nutrition 17 (5): 381–4.
  9. Ashmead, H. DeWayne (1989). 'Conversations on Chelation and Mineral Nutrition', Keats Publishing.
  10. Dietary Reference Intakes: Elements. (PDF) The National Academies. URL accessed on 2008-05-21.
  11. Iron Deficiency Anemia. (web page) MediResource. URL accessed on 2008-12-17.

Key texts


  • Bartzokis, G., Tishler, T. A., Shin, I.-S., Lu, P. H., & Cummings, J. L. (2004). Brain Ferritin iron as a risk factor for age at onset in neurodegenerative diseases. New York, NY: New York Academy of Sciences.
  • Dobson, J. (2004). Magnetic iron compounds in neurological disorders. New York, NY: New York Academy of Sciences.
  • Honda, K., Casadesus, G., Petersen, R. B., Perry, G., & Smith, M. A. (2004). Oxidative stress and redox-active iron in Alzheimer's disease. New York, NY: New York Academy of Sciences.
  • Honig, A. S., & Oski, F. A. (1986). Solemnity: A clinical risk index for iron deficient infants. Amsterdam, Netherlands: Gordon and Breach Publishers.
  • Johnson, M. A., Kuo, Y. M., Westaway, S. K., Parker, S. M., Ching, K. H. L., Gitschier, J., et al. (2004). Mitochondrial localization of human PANK2 and hypotheses of secondary iron accumulation in pantothenate kinase-associated neurodegeneration. New York, NY: New York Academy of Sciences.
  • Levine, S. M., & Chakrabarty, A. (2004). The role of iron in the pathogenesis of experimental allergic encephalomyelitis and multiple sclerosis. New York, NY: New York Academy of Sciences.
  • Pinero, D. J., & Connor, J. R. (2005). Iron and Brain Function. Philadelphia, PA: Taylor & Francis.
  • Ponka, P. (2004). Hereditary causes of disturbed iron homeostasis in the central nervous system. New York, NY: New York Academy of Sciences.
  • Requintina, P. J., & Oxenkrug, G. F. (2007). Effect of luzindole and other melatonin receptor antagonists on iron- and lipopolysaccharide-induced lipid peroxidation in vitro. Malden, MA ; New York, NY: Blackwell Publishing; New York Academy of Sciences.
  • Richardson, D. R. (2004). Novel chelators for central nervous system disorders that involve alterations in the metabolism of iron and other metal ions. New York, NY: New York Academy of Sciences.
  • Weight, L. M., & Noakes, T. D. (1994). Physical activity and iron metabolism. Champaign, IL, England: Human Kinetics Publishers.
  • Xu, X., Pin, S., Gathinji, M., Fuchs, R., & Harris, Z. L. (2004). Aceruloplasminemia: An inherited neurodegenerative disease with impairment of iron homeostasis. New York, NY: New York Academy of Sciences.
  • Youdim, M. B. H., Stephenson, G., & Shachar, D. B. (2004). Ironing iron out in Parkinson's disease and other neurodegenerative diseases with iron chelators: A lesson from 6-hydroxydopamine and iron chelators, desferal and VK-28. New York, NY: New York Academy of Sciences.


Additional material


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