Hemosiderin

HEMOSIDERIN, an iron-containing pigment formed during the breakdown of blood, more precisely, during the splitting of hematin (C₃₂H₃₂N₄O₄Fe), which in the final stage of its decomposition yields bilirubin (C₃₃H₃₆N₄O₆) and iron (Fe). The designation was proposed by Neumann. Hemosiderin appears to be a colloidal substance, only weakly bound to a protein or lipoid molecule. Accordingly, it is found both as a substance diffusely impregnating tissues and cells, and in the form of clumps (in connective tissue) and grains (in cells). Some authors consider hemosiderin to be a ferric oxide hydrate. Its color can represent all transitions from golden-yellow to dark brown. However, colorless hemosiderin is also encountered, which is revealed only microchemically. The latter phenomenon depends, according to Hueck, on the insignificance of the pigment contained in the given case. With regard to histological stains and reactions, hemosiderin behaves as follows: negative to Nile Blue, Neutral Red, Sudan III, Scharlachrot, and Ciaccio; positive to Fischler's, Smith-Dietrich's, and Weigert's (for myelin fibers) stains, which color hemosiderin dark violet. Ehrlich's hematoxylin sometimes colors it in the same hue. More often, however, hemosiderin retains its natural color with this stain. Osmium and silver nitrate do not alter it. Microchemical properties: hemosiderin is soluble in acids and insoluble in alkalis, is destroyed by chlorine, is not decolorized by anything, and according to the latest views (especially Hueck's), always gives a positive reaction for iron. There is, however, an opinion that in certain stages of development and existence of hemosiderin, the reaction for iron may be absent. The most common reaction is with potassium ferrocyanide + hydrochloric acid (Perles), in which hemosiderin is stained a bright blue color of Prussian blue [see separate plate (pp. 323–334), Fig. 6]. Another method—Quincke's—reveals iron by converting it into a black sulfur compound through the action of ammonium sulfide. Hemosiderin is formed in any pathological extra- and intravascular destruction of blood, a necessary condition for its formation being the presence of living tissue in the neighborhood and the influence of the latter—apparently through oxidation processes—upon the hematinogenic metamorphosis. This explains why in small hemorrhages per diapedesin always only hemosiderin is formed, whereas in large extravasates (and thrombi): hematoidin in the center, and hemosiderin only at the periphery, adjacent to living tissue. In intravascular erythrocyte breakdown, hemosiderin circulating in the blood is captured by the entire macrophage system of the organism and partly by parenchymal cells and accumulates in the corresponding cellular elements. This phenomenon is called hemosiderosis. It is particularly pronounced in pernicious anemia, hemochromatosis, poisoning with toluylenediamine and arsine, carcinomas, malaria, pedatrophy, hemolytic jaundice, and some other diseases.