[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [Biochemistry](https://durgical.com/en/biochemistry/) › Iron [Biochemistry](https://durgical.com/en/biochemistry/) · Topic # Iron Iron carries oxygen in haemoglobin and moves electrons in mitochondria; the body has no way to excrete it, so it controls absorption. Updated 2026-11-01 ## Key facts - About two thirds of body iron is in haemoglobin; the rest is in ferritin (storage), myoglobin and enzymes (cytochromes, catalase). - There is no regulated excretion route: balance is set at duodenal absorption, and liver hepcidin is the brake. - Low serum ferritin is the most specific sign of iron deficiency; ferritin rises with inflammation. - Iron deficiency is the world's most common nutritional deficiency and the leading cause of anaemia. ## In detail - Sources: heme iron (meat, organ meats, fish), which is well absorbed, and non-heme iron (legumes, leafy greens, fortified cereals), which is poorly absorbed. Vitamin C helps; phytates, tea, coffee and calcium hinder. - Absorption in the duodenum: ferrireductase (duodenal cytochrome b) reduces Fe³⁺ to Fe²⁺; DMT1 brings it into the enterocyte; ferroportin exports it to blood; hephaestin (a copper enzyme) oxidises it back to Fe³⁺. - Transport and storage: transferrin carries two Fe³⁺; cells take it up via the transferrin receptor; it is stored in ferritin (and haemosiderin) in the liver, spleen and marrow. - Regulation: hepcidin binds ferroportin and destroys it, closing the exit of iron from gut and macrophages. It rises with high iron and inflammation (IL-6); it falls with anaemia, hypoxia and active erythropoiesis. - Deficiency: losses (heavy periods, gut bleeding, parasites), pregnancy and growth, poor diet, malabsorption (coeliac disease, gastrectomy). Microcytic hypochromic anaemia, fatigue, pica, spoon nails, cheilitis. - Excess: hereditary haemochromatosis (low hepcidin, HFE gene), repeated transfusions, tablet poisoning in children; damages liver, pancreas, heart and joints. - Lab: ferritin, serum iron, transferrin or total iron-binding capacity (TIBC), transferrin saturation; blood count with low MCV and MCH and high RDW. **Also called** Fe, Heme and non-heme iron, Ferritin, Transferrin, Hepcidin ## Clinical notes - Iron deficiency: low ferritin, high TIBC, low saturation. Anaemia of inflammation: normal or high ferritin, low TIBC, because hepcidin is high. - In iron deficiency anaemia in an adult (especially a man or a postmenopausal woman) gut bleeding is sought, including colorectal cancer. - Iron poisoning in children who swallow tablets is an emergency: bloody vomiting, shock and liver failure; the chelator is deferoxamine. ## Drugs that act here - [Deferoxamine](https://durgical.com/en/pharmacology/deferoxamine/) - [Ferrous sulfate](https://durgical.com/en/pharmacology/ferrous-sulfate/) - [Iron sucrose](https://durgical.com/en/pharmacology/iron-sucrose/) ## Related conditions - [Iron deficiency anaemia](https://durgical.com/en/conditions/iron-deficiency-anaemia/) - [Coeliac disease](https://durgical.com/en/conditions/coeliac-disease/) - [Chronic kidney disease](https://durgical.com/en/conditions/chronic-kidney-disease/) ## Related - [Hemoglobin and 2,3-BPG](https://durgical.com/en/biochemistry/enzymes/hemoglobin-and-2-3-bpg/) - [Vitamin C (ascorbic acid)](https://durgical.com/en/biochemistry/molecules/vitamin-c/) - [Copper](https://durgical.com/en/biochemistry/topics/copper/) - [Succinate dehydrogenase (complex II)](https://durgical.com/en/biochemistry/enzymes/succinate-dehydrogenase/) ## Test yourself Think of the answer, then tap the question to see it. ## Which hormone controls iron absorption, and how? Hepcidin, from the liver: it binds ferroportin and degrades it, so iron cannot leave enterocytes or macrophages. ## Which lab pattern separates iron deficiency from anaemia of inflammation? Deficiency: low ferritin and high TIBC. Inflammation: normal or high ferritin and low TIBC. ## Why does vitamin C improve non-heme iron absorption? It reduces Fe³⁺ to Fe²⁺, the form the DMT1 transporter carries into the enterocyte. ## Why is copper needed for iron metabolism? Hephaestin and ceruloplasmin are copper ferroxidases that oxidise Fe²⁺ to Fe³⁺ so it can load onto transferrin. [Add to my cards (4)](https://durgical.app/estudiar/?add=/en/biochemistry/topics/iron/) Educational information, not medical advice. For any symptom, see a health professional. Sources: [Iron in diet: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/002422.htm) (MedlinePlus, US National Library of Medicine, 2026); [Iron Tests: MedlinePlus Medical Test](https://medlineplus.gov/lab-tests/iron-tests/) (MedlinePlus, US National Library of Medicine, 2026); [Ferritin Blood Test: MedlinePlus Medical Test](https://medlineplus.gov/lab-tests/ferritin-blood-test/) (MedlinePlus, US National Library of Medicine, 2026); [HAMP gene: MedlinePlus Genetics](https://medlineplus.gov/genetics/gene/hamp/) (MedlinePlus, US National Library of Medicine, 2026); [SLC40A1 gene: MedlinePlus Genetics](https://medlineplus.gov/genetics/gene/slc40a1/) (MedlinePlus, US National Library of Medicine, 2026); [Anaemia](https://www.who.int/news-room/fact-sheets/detail/anaemia) (World Health Organization, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011). 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