Experimental Hemosiderosis. ∗

Abstract

Many pathologists have assumed that hemosiderin is a product in the partial degradation of hemoglobin. It is recognized mostly as phagocyted material of a yellowish-brown color within mononuclear phagocytes, liver cells, or cells of the kidney tubules. It yields a Prussian blue reaction when tissues containing it are treated with acidified potassium ferrocyanide. The substance is therefore iron-containing in distinction to hematoidin. Brown 1 pointed out a number of years ago that hemosiderin-like products can be obtained experimentally by the injection of hematin derivatives. These substances he termed hemosideroid, for he found that they were soluble in hydrogen peroxide or in potassium hydrate. True hemosiderin was found to be insoluble when treated with these agents. Sprunt 2 and more recently Whipple 3 have pointed out the possibility that hemosiderin may be the result of a change in the fundamental pigment metabolism of the organism rather than a product in the partial degradation of hemoglobin.

For the past few years the writer 4 , 5 , 6 , 7 has demonstrated, in studies on inflammation and tuberculosis, that following intravenous injections of ferric chloride, the iron salt accumulates at the site of an acutely inflamed area; and in tuberculous rabbits, within the tubercles themselves, when the injections are given repeatedly. Concomitantly with this accumulation the life span of experimental rabbits is prolonged and the course of their disease is protracted. The ferric chloride when injected in the circulation forms a ferric proteinate precipitate which, in the concentration of the salt employed (0.25%), immediately redissolves. The writer 6 pointed out that hemosiderin-like granules were frequently found in the spleen, liver, bone marrow, and at times in the kidney tubules of rabbits repeatedly injected with ferric chloride.