Hemosiderin

Histopathology of a case of chronic pulmonary congestion, showing interstitium with hemosiderin deposition (black arrow), edema and collagenous thickening. The alveolus contains a siderophage (white arrow, characterized by coarse brown pigment, which is slightly refractile).
Hemosiderin image of a kidney viewed under a microscope. The brown areas represent hemosiderin

Hemosiderin or haemosiderin is an iron-storage complex that is composed of partially digested ferritin and lysosomes. The breakdown of heme gives rise to biliverdin and iron.[1][2] The body then traps the released iron and stores it as hemosiderin in tissues.[3] Hemosiderin is also generated from the abnormal metabolic pathway of ferritin.[3]

It is only found within cells (as opposed to circulating in blood) and appears to be a complex of ferritin, denatured ferritin and other material.[4][5] The iron within deposits of hemosiderin is very poorly available to supply iron when needed. Hemosiderin can be identified histologically with Perls' Prussian blue stain; iron in hemosiderin turns blue to black when exposed to potassium ferrocyanide.[6] In normal animals, hemosiderin deposits are small and commonly inapparent without special stains. Excessive accumulation of hemosiderin is usually detected within cells of the mononuclear phagocyte system (MPS) or occasionally within epithelial cells of the liver and kidney.

Several disease processes result in deposition of larger amounts of hemosiderin in tissues; although these deposits often cause no symptoms, they can lead to organ damage.

Hemosiderin is most commonly found in macrophages and is especially abundant in situations following hemorrhage, suggesting that its formation may be related to phagocytosis of red blood cells and hemoglobin. Hemosiderin can accumulate in different organs in various diseases.

Iron is required by many of the chemical reactions (i.e., oxidation-reduction reactions) in the body but is toxic when not properly contained. Thus, many methods of iron storage have developed.

  1. ^ "Hemosiderin". Definition, Staining, Function and Treatment. 2019-05-04. Retrieved 2019-05-04.
  2. ^ Kalakonda, Aditya; John, Savio (2018-10-27). "Physiology, Bilirubin". NCBI Bookshelf. PMID 29261920. Retrieved 2019-05-04.
  3. ^ a b Litwack, Gerald (2018). "Micronutrients (Metals and Iodine)". Human Biochemistry. Elsevier. pp. 591–643. doi:10.1016/b978-0-12-383864-3.00019-3. ISBN 978-0-12-383864-3. S2CID 90250940.
  4. ^ Richter, Goetz (1 August 1957). "A Study of Hemosiderosis with Aid of Electron Microscopy". The Journal of Experimental Medicine. 106 (2): 203–218. doi:10.1084/jem.106.2.203. PMC 2136742. PMID 13449232.
  5. ^ Fischbach, FA; Gregory, DW; Harrison, PM; Hoy, TG; Williams, JM (December 1971). "On the structure of hemosiderin and its relationship to ferritin". Journal of Ultrastructure Research. 37 (5): 495–503. doi:10.1016/S0022-5320(71)80020-5. PMID 5136270.
  6. ^ Kumar, Abbas, Aster, Vinay, Abul K., Jon C. (2015). Robbins & Cotran Pathologic Basis of Disease, 9th Edition. Elsevier. p. 650. ISBN 978-1-4557-2613-4.{{cite book}}: CS1 maint: multiple names: authors list (link)