596 XII. HEMOGLOBIN CATABOLISM, II 



3.4.4. Porphyrin in Lead Intoxication. In spite of the fact that 

 the porphyrin excreted in lead poisoning is predominantly of type III, 

 there is clear evidence that lead causes porphyrin formation by a 

 derangement of hemoglobin synthesis. 



Van den Bergh and Hyman {231) assumed that the porphyrin was formed 

 from hemoglobin in the liver. Schreus and Carrie (2400) and Vigliani (2882, 

 2883) found a parallel between erythrocyte destruction and porphyrin 

 formation. 



Vigliani and Angeleri (2883) assume that the plasma porphyrin found in 

 lead poisoning is derived from hemolysis, and that the porphyrin is proto- 

 porphyrin if the hemolysis is rapid, coproporphyrin if it is slow and the liver 

 has time to convert proto- to coproporphyrin. It has been claimed that lead 

 acts on the erythrocyte membrane, increasing hemolysis by changing the 

 permeability of the red cell wall (95,2081). 



Hemolysis is. however, by no means a general feature of lead poisoning 

 (cf. Vannotti, 2850; Maugeri. 188()); Francke and Litzner (945), Watson 

 (2086) and Rimington (2250) found no increase of urobilinogen excretion by 

 lead. According to Francke and Litzner. porphyrin excretion still remains 

 high after the disappearance of the anemia, and becomes normal only a few 

 weeks afterward, when increased hemopoiesis slows down. If hemoglobin is 

 injected intravenously in patients with lead poisoning, the excretion of 

 bilirubin is increased, while that of porphyrin is not affected (Kark and 

 Meiklejohn, 1468). On the other hand, bleeding strongly increases the 

 porphyrinemia and also the proto- and coproporphyrin content of the bone 

 marrow (de Langen and Grotepass, lOJfl). 



The theory of the liemolytic origin of the plasma porphyrin does not 

 account for the presence of protoporphyrin in increased amounts in the 

 erythrocytes, and postulates the conversion of protoporphyrin into copro- 

 porphyrin for which there is no evidence. Emminger and Battistini (686) 

 found fluorescent erythroblasts in the bone marrow (cf. also 1()41)- In 

 Chapter XIII it will be shown that the porpliyrin in the fluorescytes is 

 formed during hemoglobin synthesis. 



Duesberg (638) and Rimington (2259) assume that the incorporation of 

 iron into hemoglobin is inhibited by lead; cf. also Watson (2089, p. '2498). 

 This theory will be discussed further in Chapter XIII. 



3.4.5. Porphyrin Formation by Aromatic Amino Compounds. 



Rimington {2264;'2271) and Brownlee {357) have studied the influ- 

 ence of a large number of aromatic amino compounds, e.g., acetanilide, 

 phenacetin, amidopyrine, aspirin, p-aminophenol, sulfonamides, and 

 a few nitro compounds on porphyrin metabolism, and have found 

 that the ability of these substances to cause formation of hemoglobin 

 from hemoglobin is parallel to their ability to cause porphyrinuria in 

 rats. 2-Methyl-l,4-naphthoquinone is another substance which 

 causes hemiglobinemia as well as porphyrinuria {1566). Exceptions 



