ENDOGENOUS PORPHYRIN METABOLISM 583 



after protoporphyrin ingestion, as well as of the transformation of proto- 

 porphyrin to "coproporphyrin" by the liver, claimed by van den Bergh 

 (cf. below). The influence of meat diet may be indirect, for instance, by an 

 alteration of bacterial flora synthesizing coproporphyrin. The investigations 

 quoted in the preceding paragraph were carried out in the years 1923-1926, 

 at a time when the distinction between the various porphyrins was just being 

 worked out, and when Fischer still assumed coproporphyrin to be the iron- 

 free prosthetic group of myohemoglobin. It is evident that he later con- 

 sidered the results doubtful. In recent experiments, Zeligman {3173) found 

 no evidence for an increase of urinary coproporphyrin excretion in the rat 

 after injection of protoporphyrin. 



Van den Bergh and co-workers {222,229) found that lead, arsphenamine, 

 and mercury increased the protoporphyrin content of erythrocytes in parallel 

 with the coproporphyrin excretion in the urine. Chalmers and co-workers 

 {Ji.21) suggest that formic acid formed from methyl chloride may cause the 

 transformation of oroto- to coproporphyrin, and thus cause the increased 

 coproporphyrin III excretion in this disease; this can, however, be interpreted 

 differently {cf. Chapter XIII). 



Finally van den Bergh and co-workers {229) found coproporphyrin 

 in addition to protoporphyrin in rabbit bile, after perfusion of the 

 liver with defibrinated blood containing protoporphyrin. This 

 important experiment of van den Bergh could, however, not be con- 

 firmed by several workers. Vigliani {2882) found only protoporphyrin 

 to be excreted in the human fistula bile. Watson and co-workers 

 {2997) recovered only 2% of the protoporphyrin (injected intrave- 

 nously or subcutaneously) in the coproporphyrin fraction of dog bile, 

 and this consisted of coproporphyrin I and some "pseudodeutero- 

 porphyrin." After injection of protoporphyrin into the portal vein 

 of rabbits Salzburg and Watson {2I^2I^) found no coproporphyrin in 

 bile or feces. 



The parallelism of erythrocyte protoporphyrin and urinary copro- 

 porphyrin has also not been confirmed by Seggel {2527). In remission 

 from pernicious anemia, for instance, a high protoporphyrin content 

 of the erythrocytes goes hand in hand with a decrease of copropor- 

 phyrin excretion in urine and feces (Dobriner and Barker, 601). The 

 coproporphyrin in pernicious anemia and other diseases is of type I 

 and could not have been derived from protoporphyrin {cf. below). 



The question of the ultimate fate of the protoporphyrin in the 

 corpuscles must be left open; it may be excreted as such, converted 

 into coproporphyrin, or destroyed. 



3.2.5. Influence of Liver and Kidney on Urinary Porphyrin Excretion. 



Urinary porphyrin excretion has more often been determined quantitatively 



