584 XII. HEMOGLOBIN CATABOLISM, II 



than fecal excretion. Tliis is not only due to the greater ease with which 

 urinary porphyrin can be estimated, but also to the fact that the fecal 

 porphyrin is not solely derived from endogenous metabolism (c/. Section 3.3.) 

 and depends on the diet. 



Unfortunately urinary porphyrin excretion cannot be considered a safe 

 measure of porphyrin formation, since it is influenced by the state of liver 

 and kidney, particularly of the former. A damaged liver excretes the por- 

 phyrin less readily into the bile and hence more passes into the general circu- 

 lation and is excreted in the urine. The normal ratio of urinary to fecal 

 porphyrins was found to be 0.07 to O.'ii by Nesbitt and Snell {2039) and 

 somewhat higher (0.'^ to 0.6) by other workers {367,1707). In liver diseases 

 it is increased to 0.8 to 22.0. It is, for instance, increased in biliary obstruc- 

 tion and returns to normal after relief by operation. Conversely, a badly 

 diseased kidney is unable to excrete porphyrin (Nesbitt, 2037). Since por- 

 phyrinuria is often absent in pernicious anemia (Hopkins, 1333; Garrod, 981) 

 and, when it occurs, is often accompanied by urobilinuria {890,2985), Watson 

 believes that liver disturbance plays a role in causing porphyrinuria in this 

 disease. Liver disturbance is also the cause of the porphyrinuria in alcoholic 

 pellagra {2272). 



There is, however, a real increase of porphyrin formation in liver diseases 

 in addition to the proportionally larger excretion through the kidney (c/. 

 ^06,1630,2798,2976). 



3.2.6. Porphyrin Metabolism in Other Species. Some mam- 

 mals have a porphyrin metabolism very diflFerent from that of man. 

 This seems to be particularly true of rodents. In the fox squirrel, 

 Sciurus niger, for instance, porphyrin rrietabolism is similar to that 

 of a patient with congenital porphyria rather than to the normal 

 human metabolism (Turner, 2836). More attention should be paid 

 to the fact that the porphyrin metabolism of rats and mice is also 

 remarkably diflFerent from that in humans. 



Comparatively large amounts of porphyrin (about 300 ng.) are 

 found in the Harderian gland of the rat eye {561,2798,2821), the 

 gland of the female rat being richer in porphyrin than that of the 

 male {2688). According to the careful study of Thomas {2798) the 

 porphyrin is synthesized in the gland itself, while in anemia it acts 

 as a reserve store for hemoglobin synthesis. The protoporphyrin 

 which is always found in rat feces {1379,1713,2270,21^78) may origi- 

 nate in the Harderian gland. 



"Blood-caked whiskers" is another phenomenon of porphyrin metabolism 

 connected with the Harderian gland; the relation of this to protoporphyrin 

 formation in the gland is not yet clear. Chick and co-workers {J^36) and 

 Tashiro and co-workers {2740) found that the "blood-caked whiskers" of 

 the rat are .not due to hemoglobin as was previously assumed, but to por- 



