THE CHEMISTRY OF THE ANIMAL BODY. 973 



is soluble 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. As it is not decomposed by boiling, ferratin is found in the usual 

 cooked meat. Concerning the influence of inorganic salts, Schmiedeberg 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 * 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- 

 ization, was deposited in the liver and gradually excreted through the bile, 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 only 

 proof of the absorption of inorganic salts emanates from Macallum, 8 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 precipitated by the alkali of the intestines, but where the iron salt was in suf- 

 ficient quantity to neutralize the intestinal alkali it could be absorbed the whole length of 

 the small intestines. Whether inorganic iron unites with proteid before absorption or not 

 is unknown. 



Regarding the transformation of iron compounds after absorption into haemoglobin, 

 little is known except that the necessary synthesis takes place in the 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 and spleen, this 

 being noticeable in pernicious anaemia. On the production of icterus with arseniuretted 

 hydrogen, similar iron compounds are noted in the liver, being cleavage products of haemo- 

 globin in its transformation to biliary coloring matter. The amount of iron normally 

 excreted from the body is far less than the corresponding biliary coloring matter (see 

 Haemochromogen), showing that the rest of the iron is retained for further use in con- 

 structing new haemoglobin. 



Iron is excreted as phosphate in the gastric juice, in bile (in considerable quantity), and, 

 according to Macallum, 7 in the intestinal juice. In the urine it is present as an unknown 

 organic compound. 



A newborn child or animal has, proportionately to its weight, far more iron than at any 



1 Marfori, loc. cit., and Schmiedeberg, Archiv fur exper. Pathologic und PharmaJcologie, 1894, 

 Bd. 33, p. 101. 



2 Vay : Zeitschrift fur physiologische Chemie, 1895, Bd. 20, p. 398. 



3 Schmiedeberg, Op. cit., p. 110. 



* Zeitschrift filr physiologische Chemie, 1891, Bd. 15, p. 371. 



5 Pfluger's Archiv, 1891, Bd. 50, p. 11. Journal of Physiology, 1894, vol. 16, p. 268. 



T Op. cit., p. 278. 



