THE CHEMISTRY OE THE ANIMAL BODY. 529 



prepared a substance from proteid and iron salts, called ferratin, which contains 4 to 8 

 per cent, of iron ; it is a compound unaffected by gastric juice or by boiling ; it is solu- 

 ble in the alkaline intestine, where it is but slowly affected by alkaline sulphide. Now 

 this same ferratin is found in the body itself, especially in the liver, 1 although not the only 

 iron-containing substance of the liver. 2 If ferratin be fed, the quantity of it increases in 

 the liver. If a dog be fed on milk, which is always poor in iron, and he be bled from 

 time to time, the ferratin disappears from the liver, being used for the formation of new 

 red blood-corpuscles. 3 Such a liver does not change color when placed in dilute ammo- 

 nium sulphide, while one containing ferratin or other iron compounds gradually turns black 

 from iron sulphide. If milk containing ferratin be fed, the ferratin may be deposited in 

 the liver for the use of the blood. As it is not decomposed by boiling, ferratin is found in 

 the usual cooked meat. Concerning the influence of inorganic salts, Selimiedeberg agrees 

 with Bunge that the formation of iron sulphide protects the ferratin from attack. 



The insolubility of iron salts in alkaline solutions has raised the question of their 

 absorption by the blood. If inorganic iron salts be injected into a vein, the iron reappears 

 chiefly in the intestines, with only 3 to 4 per cent, in the urine (Jakobj): in too great 

 quantities they have powerful toxic properties. Gottlieb 4 administered 0.1 gram of iron 

 as sodium iron tartrate subcutaneously to a dog during a period of nine days ; twenty-eight 

 days after the first injection 0.0969 gram Fe had been removed in the excreta over and 

 above the normal excretion calculated for the same time. It was shown that this iron was 

 especially stored in the liver. It may be argued that such iron, being foreign to the organ- 

 ism, was deposited in the liver and gradually excreted as other heavy metals, mercury, 

 copper, lead, would be. Kunkel 5 fed mice and to the food of half their number added a 

 solution of oxychloride of iron (FeCl 3 ,4Fe(OH) 3 , liquor ferri oxychlorati) : in the livers of 

 those fed with iron, iron was present to a greater extent than in the others ; but here, 

 again, the surplus can be attributed to the sulphide-forming protective power of the added 

 salts, which Kunkel admits, though maintaining the contrary ground. The proof of the 

 absorption of inorganic salts emanates from Macallum, 6 who showed, after feeding chloride, 

 phosphate, and sulphate to guinea-pigs, that the epithelial cells and the subepithelial 

 leucocytes of the intestines gave a strong microchemical reaction for iron with ammonium 

 sulphide. With small doses this was observed only near the pylorus, for iron is soon pre- 

 cipitated by the alkali of the intestines, but where the iron salt was in sufficient quantity 

 to neutralize the intestinal alkali it coidd be absorbed the whole length of the small intes- 

 tine. Whether inorganic iron unites with proteid before absorption or not is unknown. 

 According to Swirski, the absorbed iron compounds pass into the lymph or into the blood 

 of the portal vein. In the latter they are taken up by the leucocytes (phagocytes) and 

 carried to the liver. Fasting guinea-pigs which have been prevented by muzzling from 

 eating their feces and thus deprived of even a small quantity of iron, are more susceptible 

 to disease than the same unmuzzled annuals. The iron-containing phagocytes are believed 

 to destroy bacterial poisons. 



Regarding the transformation of iron compounds after absorption into haemoglobin, 

 little is known except that the necessary synthesis takes place in tin' spleen, in the bone- 

 marrow, and probably in the liver. On the destruction of red blood-corpuscles, proteid 

 bodies holding iron in combination are deposited in the cells of the liver, spleen, bone- 

 marrow, and kidney, 7 this being noticeable in pernicious anaemia. On the production of 



1 Marfori, he. cit, and Selimiedeberg, Archiv fiir exper. Pathologie mid Pharmakohgie, 1894, 

 Bd. 33, S. 101. 



' Vav : Zeitschrift fur physiologisehe Chemie, 1895, Bd. 20, S. 398. 



3 Schmiedeberg, Op. cit., S. 110. 



* Zeitschrift fiir physiologische Chemie, 1891, Bd. 15, S. 371. 



5 Pjliiger's Archiv, 1891, Bd. 50, S. 11. 



6 Swirski: Ibid., 1899, Bd. 74, S. 4G6 ; Journal of Physiology, 1894, vol. 16, p. 268. 

 1 Schurig; Archiv fur exper. Pathologic nml Pharmabtlmjir, lS'.ts, p,J. 41, s. 29. 



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