iron metabolism


Also found in: Encyclopedia.

iron metabolism

a series of processes involved in the entry of iron into the body and its absorption, transport, storage, use in the formation of hemoglobin and other iron compounds, and eventual excretion. Iron normally enters through the intestinal mucosa and is oxidized from ferrous to ferric iron in the process. The rate at which iron enters is modulated by this absorption mechanism. When iron stores are high, iron no longer passes through but is trapped by the mucosal cells of the intestine to be eliminated. Once in the blood, iron cycles between the plasma and the reticuloendothelial or erythropoietic system. For hemoglobin synthesis, plasma iron is delivered to the normoblast, where it remains up to 4 months, functioning in the hemoglobin molecules of a mature red cell. Senescent red cells then deteriorate. The iron is released from the hemoglobin by the reticuloendothelial system to reenter the transport pool for recycling. The normal iron distribution in a 70-kg adult (male) totals approximately 3.7 g, more than 65% in circulating hemoglobin. Another 27% is found in the storage pool as hemosiderin or ferritin. The body normally conserves iron so well that loss, usually only through the feces, is normally limited to about 1 mg/day. This amount is easily provided by a dietary intake of only 10 mg/day. Iron deficiency may follow extended intervals of inadequate iron intake (especially in women), in pregnancy when higher levels of iron are needed, or with excessive blood loss. Iron overload sometimes occurs in disorders in which normal regulation of iron absorption is impaired, called hemochromatosis. Hemochromatosis may be inherited or acquired in long-term transfusion therapy for chronic anemias. See also anemia, hemochromatosis, iron deficiency anemia, iron transport.

iron me·tab·o·lism

(ī'ŏrn mĕ-tab'ŏ-lizm)
The sum of the chemical and physical processes whereby iron is introduced into or evacuated from the body.
References in periodicals archive ?
Under conditions where iron metabolism is disturbed, such as in transfusion-dependent patients with thalassemia major, myelodysplastic syndromes, aplastic anemia, or sickle cell disease, excessive iron deposition occurs in the liver, heart, and endocrine organs, resulting in reactive oxygen species (ROS) through the Fenton and Haber–Weiss reaction.
Hepcidin (Hep), ferroportin-1(Fpn-1) and transferrin (Tf) are the important proteins associated with iron metabolism and the onset of acute phase response (APR) influences their gene expressions.
Anemia, ineffective erythropoiesis, and hepcidin: interacting factors in abnormal iron metabolism leading to iron overload in [beta]-thalassemia.
Key considerations involve attention to hepatic and renal pathologies, alimentary and lifestyle inventories, toxic and immunological burdens, and genetic predispositions that may amplify or promote an iron metabolism dysfunction.
The expression of several genes involved in iron metabolism including lactotransferrin, ceruloplasmin ferroxidase, lipocalin 2 and ferroportin [12] upregulate during uterine growth and differentiation.
In the previous studies, it has been reported that effect of chelating agents on iron metabolism as anti-tumor agents in cancer cells [9,10].
Kikuchi, "Dysregulation of iron metabolism in Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis," Advances in Pharmacological Sciences, vol.
Iron regulatory proteins and their role in controlling iron metabolism.
The challenging task of maintaining intracellular iron levels sufficient for essential cellular functions, including ROS-dependent cell signaling, but as low as possible to avoid ROS-mediated injury, is controlled at multiple steps but primarily accomplished by iron regulatory proteins (IRP1 and IRP2), which strictly control intracellular iron metabolism by posttranscriptionally regulating the coordinated expression of proteins involved in iron utilization (e.
Here, the role of genes involved in iron metabolism and homeostasis for the cytotoxicity of ten artemisinin derivatives have been systematically investigated.
The bronzing of the skin in a diabetes patient can be a sign of an inherited defect in iron metabolism that leads to liver failure known as hemochromatosis.