58 METABOLISM OF ORGANIC AND INORGANIC PHOSPHORUS. 



is induced. Ltisk a offers the following general hypothesis as his expla- 

 nation of fatty changes in tissues: 



The lactic acid which occurs is derived from the sugar formed in proteid metabolism. 

 In the above case the sugar is removed before its conversion into lactic acid. In 

 phlorhizin diabetes, dextrose does not burn; in phosphorus poisoning lactic acid 

 derived from dextrose does not burn. In both cases a sugar-hungry cell, or one where 

 carbohydrate is not oxidized, is found, and under these circumstances fat is attracted 

 to the cell, and in larger quantities than can be useful. Wherever sugar freely burns 

 this fatty infiltration is impossible. A reduced local circulation in a portion of the 

 heart may produce anemia of the part, an imperfect local combustion of lactic acid 

 normally formed and a fatty infiltration of the locality. 



******* 



It has been stated that the action of phosphorus is to induce autolysis (self-digestion) 

 of the body's protoplasm (Jacoby, 6 Waldvogel c ), since leucin, tyrosin, and other 

 amino acids may be eliminated in considerable quantity in the urine. Oswald & 

 thinks that phosphorus destroys or weakens the antiautolytic agents of the body. 

 That autolytic enzymes do not gain free control over the cells through the direct 

 influence of phosphorus is proved by the work of Ray, McDermott, and Lusk. 

 These authors found that phosphorus injections raised the proteid metabolism of fasting 

 dogs to 250, 260, 283, 248, 183, and 164 per cent of that of the dog when normal. They 

 contrasted this increased proteid metabolism with that obtained in phlorhizin glyco- 

 suria, which is represented by increases to 540, 450, 340, and 340 per cent. When, 

 however, they gave phlorhizin and obtained the increased metabolism, and then 

 injected phosphorus, this was not followed by any marked increase in proteid metab- 

 olism. Under these circumstances phlorhizin glycosuria is the predominating factor, 

 removing the dextrose produced from proteid. As regards phosphorus poisoning, 

 Araki/ believes that lactic acid accumulation is due to lack of oxygenation of the 

 tissues caused by a slow heart beat, but not due to anemia. He does not believe the 

 oxygen deprivation to be very pronounced. The writer offers the explanation that 

 phosphorus may affect the enzyme which breaks up the lactic acid derived from dex- 

 trose, and the accumulation of this acid may prevent the action of some of the deni- 

 trogenizing enzymes; and further, its noncombustion may necessitate an increase of 

 proteid metabolism. 



This theory is strengthened by the discovery of Schryver g that the addition of 

 lactic acid favors the accumulation of amino acids in autolysis of the liver. 



In this connection we must recognize the fact that the presence of 

 amino bodies leucin, tyrosin, etc. in the liver in cases of phosphorus 

 poisoning is well established. Abderhalden and Bergell 71 detected 

 glycocoll in the urine of a rabbit poisoned with phosphorus. Wohl- 

 gemut-J found phenylanin and arginin in the urine after a case of phos- 

 phorus poisoning. An altered quantitative relationship between 



a The Elements of the Science of Nutrition, Philadelphia, 1906. 



bZts. physiol. Chem., 1900, SO : 174. 



cArch. klin. Med., 1905, 82 : 437. 



<*Biochem. Centrbl., 1905, 3 : 365. 



Amer. J. Physiol., 1899, 3 : 139. 



/Zts. physiol. Chem., 1893, 17 : 310. 



0Bio-Chem. J., 1906, 1 : 123. 



& Zts. physiol. Chem., 1903, 39 :464. 



'Ibid., 1905, 44:74. 



