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Cellular Components of Blood
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Almost all iron (in the ferrous [Fe2+] state) absorption occurs in the duodenum. Factors favouring the absorption of iron include gastric acid and reducing agents, which maintain the soluble iron in the ferrous state. Iron absorption is reduced by alkali and chelating agents such as phytates and phosphates, which form insoluble iron complexes. Fe2+ iron is transported into the enterocyte via divalent metal transporter 1 (DMT1) across the brush border of duodenal enterocytes. Within these cells, some Fe2+ binds to apoferritin and is stored as ferritin in the ferric [Fe3+] state and is shed into the gut lumen at the end of the lifespan of the these cells (3–4 days). The remaining Fe2+ ions are transported out of the enterocytes by ferroportin 1 in the basolateral cells of the duodenal enterocyte. In the plasma, Fe2+ is converted to Fe3+ and bound to transferrin, a plasma glycoprotein. Normally, it is about 35% saturated with iron. Normal plasma iron level is 19–23 μmol/L.
Gastroenterology
Published in Paul Bentley, Ben Lovell, Memorizing Medicine, 2019
Aet: 1°: HFE gene (esp. C282Y mutation), results in: Increased divalent-metal transporter (DMT-1) expression on brush border of enterocytesReduced hepcidin expression in liver (hepcidin inhibits iron absorption from gut)2°: Haemolytic anaemia, aplastic anaemia, sideroblastic anaemia, due to ineffective erythropoiesis and iron release, increased iron absorption, repeated blood transfusions
Micronutrients for the Prevention and Improvement of the Standard Therapy for Parkinson’s Disease
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
Several studies have confirmed that PD is associated with a significant increase in free iron in the degenerating substantia nigra.131–133 The effects of iron on degeneration of DA neurons are via increased oxidative stress. The mechanisms of accumulation of iron in the substantia nigra are unknown; however, an isoforms of the divalent metal transporter-1 (DMT1) is elevated in the substantia nigra of PD brain.134
Hyperferritinemia with iron deposition in the basal ganglia and tremor as the initial manifestation of follicular lymphoma
Published in International Journal of Neuroscience, 2023
Hussein Algahtani, Ahmed Absi, Bader Shirah, Hatim Al-Maghraby, Hussam Algarni
Iron is the second most prevalent metal on the earth and the most important element in the body. The source of iron in the body comes from a well-balanced diet that contains sufficient iron to meet body requirements. About 10% of the normal dietary iron is absorbed daily, which is sufficient to balance losses from desquamation of the epithelium. The utilization of iron increases in periods of stress or increased demands such as growth in childhood, menstruation and pregnancy in women, and subjects with chronic minor hemorrhages such as hemorrhoids and other causes of gastrointestinal loss [4]. The main site of absorption of iron in the duodenum and upper jejunum where divalent metal transporter 1 (DMT1) facilitates the transfer of iron across the intestinal epithelial cells. This transporter protein is non-specific and also facilitates the uptake of other trace metals such as manganese, copper, zinc, lead, and cadmium. Iron within enterocytes is then released via ferroportin into the bloodstream, where it is then bound by the transport glycoprotein named transferrin. Only 0.1% of the total body iron is circulating in bound form to transferrin, and most absorbed iron is utilized by erythroid precursors in the bone marrow. About 10-20% of absorbed iron is stored in the mononuclear phagocyte system. Other iron in the body is distributed between red blood cells hemoglobin, the liver, and muscles. The body has no effective means of excreting iron, and iron homeostasis is totally dependent on the regulation of the absorption of dietary iron from the duodenum [5].
A deep dive into future therapies for microcytic anemias and clinical considerations
Published in Expert Review of Hematology, 2023
François Rodrigues, Tereza Coman, Guillemette Fouquet, Francine Côté, Geneviève Courtois, Thiago Trovati Maciel, Olivier Hermine
Dietary iron absorption is usually limited to 1–2 mg per day and mainly serves in adults to compensate for losses, such as bleeding or intestinal cells desquamation [2]. The divalent metal transporter 1 (DMT1) takes up ferrous iron reduced by the duodenal cytochrome B (DCYTB) on the luminal side of enterocyte [15]. As transferrin, DMT1 mRNA possesses an IRE in its 3‘UTR, stabilizing expression during iron deprivation (Galy 2008 Cell Metabolism). DMT1 pathogenic mutations are responsible for a hypochromic microcytic anemia with slowly developing iron overload, suggesting that other absorption mechanisms, such as heme transport by duodenal Feline Leukemia Virus subgroup C Receptor 1 (FLVCR1), can compensate for DMT1 deficiency [16–18]. Indeed, microcytic anemia in this context is not caused by blood iron levels’ depletion but by inefficient iron export from endosomes to the cytosol for heme synthesis after transferrin internalization [5]. Abnormal subcellular iron localization causes ineffective erythropoiesis in this condition. Fascinatingly, erythropoietin (EPO) administration improves hemoglobin levels in patients with DMT1 deficiency [19]. This effect is mediated by inefficient erythropoiesis-linked apoptosis inhibition by EPO.
SARS-CoV-2 Infection Dysregulates Host Iron (Fe)-Redox Homeostasis (Fe-R-H): Role of Fe-Redox Regulators, Ferroptosis Inhibitors, Anticoagulants, and Iron-Chelators in COVID-19 Control
Published in Journal of Dietary Supplements, 2023
Sreus A.G. Naidu, Roger A. Clemens, A. Satyanarayan Naidu
Fe-R-H depends on the expression and activity of iron-carriers, iron-transporters, iron-regulators, and iron-storage proteins. Divalent metal transporter 1 (DMT1) located in the intestinal enterocyte sequesters non-heme iron from the diet, and ferroportin 1 (FPN1) exports iron into the circulation (28). Plasma TF and LF transport iron to various tissues and cells. After binding to transferrin receptor 1 (TfR1), the complex is endocytosed and release iron into the cytoplasm (29). Free iron is utilized either for metabolism, or sequestered by the cytosolic ferritin, as cellular iron reserve. Excess iron is exported from the cell via FPN1 and hepcidin (30). Intra-cellular IRPs modulate the expression of DMT1, TfR1, ferritin, and FPN1 via binding to the iron-responsive element (IRE) (31,32). The systemic Fe-R-H is mainly orchestrated by the hepcidin/FPN1 axis.