Body iron metabolism and pathophysiology of iron overload
Open accessAbstract
Iron is an essential metal for the body, while excess iron accumulation causes organ dysfunction through the production of reactive oxygen species. There is a sophisticated balance of body iron metabolism of storage and transport, which is regulated by several factors including the newly identified peptide hepcidin. As there is no passive excretory mechanism of iron, iron is easily accumulated when exogenous iron is loaded by hereditary factors, repeated transfusions, and other diseased conditions. The free irons, non-transferrin-bound iron, and labile plasma iron in the circulation, and the labile iron pool within the cells, are responsible for iron toxicity. The characteristic features of advanced iron overload are failure of vital organs such as liver and heart in addition to endocrine dysfunctions. For the estimation of body iron, there are direct and indirect methods available. Serum ferritin is the most convenient and widely available modality, even though its specificity is sometimes problematic. Recently, new physical detection methods using magnetic resonance imaging and superconducting quantum interference devices have become available to estimate iron concentration in liver and myocardium. The widely used application of iron chelators with high compliance will resolve the problems of organ dysfunction by excess iron and improve patient outcomes.
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Intestinal sources provide only 1-2 mg of iron per day; the daily demand for 20 mg of iron for erythropoiesis is largely met by recycled iron from senescent erythrocytes processed by the reticuloendothelial system.
“Intestinal sources provide only 1-2 mg of iron per day.The daily demand for 20 mg of iron for erythropoiesis is largely met by recycled iron from senescent erythrocytes processed by the reticuloendothelial system (RES) consisting of specialized macrophages present mainly in the liver, spleen and bone marrow.”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Kohgo et al., 2008
Unlike transferrin-bound iron, cellular uptake of NTBI is not dependent on TfR and the resulting iron is diffusely distributed throughout the organ.
“Unlike Tf-bound iron, cellular uptake of NTBI is not dependent on TfR and therefore the resulting iron is diffusely distributed throughout the organ (Kohgo et al., 2008).”
From Iron, Oxidative Stress and Health (2012) · cites this paper as Kohgo et al., 2008
Loss of iron in a typical adult male is very small and can be met by absorbing 1-2 mg of iron per day.
“However, the loss of iron in a typical adult male is very small [208,209] and can be met by absorbing just 1 – 2 mg of iron per day [210,211].”
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References 48 · Cited by 616
- Authors
- Kohgo, Y., Ikuta, K., Ohtake, T., Torimoto, Y., & Kato, J.
- Affiliations
- Asahikawa Medical University (JP)
- Sapporo Medical University (JP)
- Corresponding author
- Kohgo, Yutaka
- Venue
- International Journal of Hematology
- Published
- 2008-07
- Volume
- 88
- Issue
- 1
- Pages
- 7-15
- ISSN
- 0925-5710 (ISSN-L)
- 1865-3774
- PMC
- PMC2516548
- OpenAlex
- W1970096539
- Cited by
- 616
- References
- 48
- Citations by year
- 2026: 14 · 2025: 47 · 2024: 38 · 2023: 39 · 2022: 53 · 2021: 52 · 2020: 62 · 2019: 43 · 2018: 44 · 2017: 33 · 2016: 20 · 2015: 26 · 2014: 28 · 2013: 23 · 2012: 23
- FWCI
- 3.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- International Journal of Hematology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (20590754)
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Health Sciences › Medicine › Genetics › Hemoglobinopathies and Related Disorders
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- iron metabolism, iron overload, hepcidin, reactive oxygen species, transferrin-bound iron, labile plasma iron, labile iron pool, iron toxicity, serum ferritin, liver iron overload, cardiac iron overload, iron chelation, hereditary hemochromatosis, repeated transfusion
- MeSH terms
- Biological Transport, Ferritins, Humans, Iron, Liver, Magnetic Resonance Imaging, Myocardium, Radiography, Reactive Oxygen Species, Iron Overload, Transfusion Reaction
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