BACTERIAL METABOLISM WITHIN THE BODY 683 



Betaethyl indol 

 cH 2 CH 2 COOH > A-,CH 2 CH 3 + C0 2 



Indol acetic acid (urorosein) 

 A CH 2 CH 3 + 30 A_ CH 2 COOH + H 2 O 



yj 



v K 



Skatol 



,CH 3 + CO 2 



Betaindol formic acid 

 CH 3 + 30 = /V COOH + H 2 O 



COOH 



Indol is formed in the greatest amounts in those cases where intestinal 

 putrefaction is actively taking place. Obstruction of the small intestine 

 is a very potent factor in promoting excessive amounts (Combe). Slug- 

 gish peristalsis with the attendant relatively slow absorption of the 

 products of protein digestion provides conditions favoring an overgrowth 

 of Bacillus coli and other indol-forming bacteria. 



Gelatin, which is deficient in tryptophan [and other aromatic amino 

 acids] does not play a part in indicanuria. The toxicity of indol ap- 

 pears to be slight, and it is lessened when indol is oxidized and is paired 

 with sulphuric acid (Herter). Amounts administered by mouth to 0.2 

 gram, however, appear to cause headache, malaise and lassitude. 



Defective oxidization in the liver may lead to a low grade indol 

 toxemia. Herter and Wakeman found that surviving liver acts upon 

 indol in such a manner that it cannot be recovered by distillation of the 

 organ. The kidney and muscle are unable to fix indol in this manner. 



