Iron (Fe, atomic weight 55.847) is a metallic di- or trivalent transition element with naturally occurring stable isotopes 54 (5.8%), 56 (91.7%). 57 (2.2%), and 58 (0.33%). The artificial isotopes 52. 53. 55. 59.60. and 61 are radioactive.


DMT1 divalent metal ion transporter

HFE symbol for the hemochromatosis gene

IRE iron response element

IRE-8P iron-responsive element binding protein

IRP iron regulatory protein

Tf transferrin

TFR transferrin receptor

Nutritional summary

Function; Iron is essential as a cofaclor of oxygen transport, respiration, amino acid lipid alcohol, vitamin A. and sullite metabolism, and various other redox reactions. Requirements. At least 8 mg iron are necessary to maintain adequate stores for people consuming a mixed diet, more for women between 19 and 50 ( 18 mg/d), vegetarians, and during pregnancy (27 mg/d) and lactation (9 mg/d).

Sources: All muscle foods ;ue good iron sources. Phytate from whole grains and some vegetables interferes with iron absorption; dietary aseorbatc promotes absorption. Deficiency: Diminished stores cause loss of appetite, microcytic anemia, and impaired immune function. Deficiency slow s growth and cognitive development of infants and children. This may be partially irreversible.

Excessive intake; Greatly expanded iron stores may damage liver, pancreas, and heart. Iron supplement intake decreases the absorption of concomitantly ingested thyroxine. tetracycline derivatives, penicillamine, methyldopa, levodopa, carbidopa, and ciprofloxacin.

Dietary sources

Foods contain heme proteins (myoglobin, hemoglobin, cytochromes and a few enzymes), ferrous iron t Fe; ), and ferric iron t Fe1 ). Ferrous and ferric iron, usually called non-heme iron, comprise about 60% of the iron in meats, and most of the iron in plant-derived foods.

Iron-rich foods include all meats, such as beef (0.019 mg/g), pork (0.009 mg/g), chicken (0.0l2mg g). and lish (e.g. tuna 0.009mg/g), Legumes also are relatively iron-rich foods (e.g. baked beans 0.003 mg/g). Grains and grain products ha\ e to be fortified in the United States with 0.0044 mg/g.

While iron intakes are very commonly inadequate worldwide, typical intakes tend to be high in North America and Europe. Median daily iron consumption of American women is around 9tng (Food and Nutrition Board Institute of Medicine, 2001: Appendix E-5); median consumption of men is about 12mg.

Digestion and absorption

Uptake of iron from the intestinal lumen uses al least three distinct pathways, one for heme-bound iron through a largely uncharactcrizcd pathway, another one for ferrous iron (Fc:') % i.t the divalent metal ion transporter I (DMT I), and one for ferric iron (Fe' ) via the beta3-integrin-mobilferrin pathway (Conrad et ai. 2000). The relative contribution ofthe two non-heme iron pathways remains uncertain. Absorption is most effective in the duodenum, slightly less so in the remainder ofthe smalt intestine, and least in the colon.

Phytate and polyphenols in various commonly consumed foods and beverages strongly inhibit non-heme iron absorption (linnet et ai, 1999J. Absorption inhibitory potential is greatest for black lea (79 94%). peppermint tea (X4%). pennyroyal tea (73%), cocoa (7|%), and infusions from vervain (59%), lime Sower (52%). and chamomile (47";,). Ascorbatc, organic acids, and heme promote absorption of non-heme iron (llnrret etui., 1999),

Uptake of ferrous iron: DMTI (Nramp2. SLC11A2) transports ferrous iron (Fe*') together w ith a proton across the brush border membrane ofthe proximal small intestine (Tandy et ul.. 2000). Luminal mucin facilitates this uptake (Conrad et ai, 1991). Duodenal cytochrome b at the brush border membrane helps with the reduction of Fe1 . Uptake of ferric iron: Contrary to long-held assumptions, ferric iron can be absorbed directly from the intestinal lumen by a specific pathway that depends on beta3-intcgrin. A critical factor is the low solubility of Fe'1 at neutral to alkaline pH. Mucin and dietary chelators, such as citrate and similar organic acids, can keep this form of iron in solution and thereby greatly improve its bioavailability. Uptake of heme iron: Pathways for the uptake of heme are distinct from those for non-heme iron, but still very incompletely understood. Neither iron absorption inhibitors, such as phytate. nor absorption enhancers, such as mucin or citrate, have much effect on heme uptake. A heme-binding protein. Has Ah, contributes to transport across the brush border membrane (Castellani ei a I., 20(H)). Heme oxygenase (ECI, 14.99.3). which may also aid the transfer, releases iron from its porphyrin scaffold and converts it into Fe34 (Drummond etal., 1992).

Intracellular disposition. Iron is oxidized upon entry into the cell by as yet incompletely characterized oxidases, which might include ceruloplasmiu and hephacstin. The iron-hinding chaperone mediates cytoplasmic transport of ferric (Fe'1) iron (Conrad et ul., 1992). Some iron in the cytoplasms is stored temporarily with paraferritin, a large complex of at least 4 polypeptides including intcgrin. mobillerrin (calreticulin. rho), and a llavin This complex is also capable of reducing Fc1 to Fe:" (Umbreit et ul.. 1996). Of great importance for the regulation of ils intestinal absorption efficiency is the storage of iron with ferritin. The spherical complexes consist of 24 identical ferritin subunitsand several thousand Fe1' atoms. This type of storage holds on to the iron until the enterocyte is shed at the end of its 2-3 day life span into the intestinal lumen, and therefore effectively limits iron absorption.

Some transferrin-bound iron arrives from blood circulation via the transferrin receptor 1 (TfR 11 The receptor-lransfcrrin complexes concentrate in clathrm-coated pits and are directed to specific endosomal compartments. Iron is pumped out of the endosomal vesicles by DMTI and as yet incompletely understood mechanisms return both transferrin and TfWl to the basolateral membrane. ADP-Ribosylation factor 6 contributes to the intracellular trafficking of the transferrin-transferrin receptor complex.

Figure 11.7 Intestinal .ibsorption of iron

Export into blood: An important step he fore Fc: can leave the enterocyte is its oxidation to Fei1". Available iron-oxidizing enzymes include the ferroxidusc (EC I. I6.3.1) ceruloplasmin and a closely related protein, hephaestin. The copper-containing hep-haestin is expressed along the entire length of the small intestine (Frazeret id., 2001). Ferroportin 1 (I REG I, MTPI, SLCII A3 i finally moves iron across the basolateral membrane (Donovan et id., 2000).

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