560 XI. HEMOGLOBIN CATABOLISM, I 



Bingold has claimed that it occurs in normal plasma, but this has not been 

 confirmed by Fischer and von Dobeneck (S07). It is found in the urine in 

 most liver diseases, in hemolytic anemia, severe heart discompensation, high 

 fever, and in other diseases (ISGG) — mostly together with urobilin and bili- 

 rubin, but occasionally without these bile pigments. On the other hand, it 

 is not found in the urine of pernicious anemia in spite of the presence of 

 urobilin. Bingold assumes that it is formed by the action of hydrogen peroxide 

 on hemoglobin in the kidney, after the hemoglobin has been freed from 

 catalase whicli prevents its oxidation in the erythrocyte. It is known that 

 the kidney contains enzyme systems which produce hydrogen peroxide. 

 Nevertheless the theory has many weak points. Normally no significant 

 amount of hemoglobin ever passes the glomerulus, and it is doubtful whether 

 it does so in many of the instances in which pentdyopent was found in the 

 urine. If the theory were correct one should expect to find much pentdyopent 

 in hemoglobinuric urine, but no claim to this effect has been found. Bingold 

 observed that hemoglobin in such urines is destroyed in vitro by high con- 

 centrations of hydrogen peroxide, but this can hardly be considered as suffi- 

 cient evidence. Later Bingold {27If,27G) and Hulst and Grotepass {1366) 

 assumed that pentdyopent is formed from bilirubin in the kidney, again by 

 the action of hydrogen peroxide. 



There is little evidence that pentdyopent, even in pathological conditions, 

 contributes much to tiie products of hemoglobin destruction. The example 

 brought by Watson {29S9) shows only the normal picture, urobilin account- 

 ing for no more than two-thirds of the hemoglobin destruction. This normal 

 divergency between bilirubin and urobilin cannot be accounted for by the 

 formation of pentdyopent, since pentdyopent does not occur in normal urine. 



We have pointed out in Chapter X, Section 9., that in some cases pent- 

 dyopent may have been an artefact formed from bilirubin or mesobilane. 

 While there can be no doubt that pentdyopent occurs occasionally as a 

 pathological breakdown product of hemoglobin, its importance has been 

 exaggerated. 



Bilifiiscins. It is not yet certain whether bilifuscins {cf. Chapter IV, 

 Section 8.1., and this chapter. Section 7. .5.) occur normally in bile, as Siedel 

 assumes, or are artefacts formed from bilirubin, as Fischer is inclined to 

 believe, and whether they are derived solely from myohemoglobin, or also 

 from hemoglobin. Mesobilifuscin was found in normal feces by Meldolesi 

 {2558) (as the chromoprotein myobilin), but in insignificantly small amounts 

 compared with the bilirubin or urobilin excretion. The experiments of 

 Meldolesi, Siedel, and Moller make it appear more likely that myohemo- 

 globin, not hemoglobin, is the source, but Siedel himself leaves the question 

 open. 



Recently With {3111,3113) has claimed that bilifuscins occur in normal 

 sera and are increased in pathological conditions. In certain cases of biliary 

 obstruction and yellow atrophy of the liver, in which no jaundice was found, 

 it was assumed that hemoglobin is tran.sformed into bilifuscins instead of 

 into bilirubin.* 



♦ CJ. also With {■niia) and Lups and Meijer {178Ha). 



