WESTERN SNEEZE WEED AS A POISONOUS PLANT. 23 



Table 2. — Results of toxicity tests with dugaldin. 





Weight. 



Date. 



Dose. 



Material. 



Effect. 



Termina- 

 tion. 





Animal. 



Quan- 

 tity. 



How given. 



Autopsy. 



Guinea pig 17. 



Guinea pig 18. 

 Guinea pig 19. 



Guinea pig 20. 



Grams. 

 500 



355 

 400 



425 



1919. 

 Mar. 26 



...do.... 

 ...do.... 



...do.... 

 Mar. 27 

 Mar. 28 

 Mar. 29 

 Mar. 30 

 Mar. 27 



...do.... 



Mar. 28 



Apr. 9 

 Mar. 27 



Ml. 



4 



2 

 .5 



.5 



1 

 .5 

 .5 

 .5 



1 



1 



4 



2 

 1.5 



Orally 



do 



Subcu- 

 taneously. 



do 



do 



Solution of du- 

 galdin. 



do 



do 



do 



do 



Sick 



...do.... 



Died 



...do.... 



Charac- 

 teristic. 

 Do 



...do 



...do 



...do 



...do 



...do 



...do 



...do 



...do 



...do 



Killed 



Recovered 



...do 



...do 



...do 



...do 



...do 



...do 



...do 



Do. 







do i do 



do i do 

















Guinea pig 21. 

 Guinea pig 22. 



Guinea pig 23. 



Guinea pig 24. 

 Rabbit 21 



380 

 365 



250 



240 

 1,800 



Orally 



Subcu- 

 taneously. 

 Orally 



do 



do 



Solution pre- 

 cipitated by 

 tannic acid. 

 do 





...do 



Killed 

 ...do 



Do. 



Intrave- 

 nously. 



do 



...do 



Do. 











CHEMICAL SUMMARY. 



1 . The poisonous principle of Helenium hoopesii is an easily decom- 

 posed glucosid to which the name "dugaldin" has been given. It is 

 a bitter, white, amorphous solid; soluble in alcohol; less soluble in 

 water and chloroform; insoluble in ether, benzene, and petroleum 

 ether. 



2. Dugaldin is most poisonous when administered orally, but is 

 also toxic when given intravenously, subcutaneously, or rectally. 



3. Dugaldin may be precipitated from its solutions by tannic acid, 

 with which it forms a sparingly soluble compound of low toxicity. 



4. Helenic acid, the active principle of Helenium autumnale, does 

 not occur in H. hoopesii, nor do alkaloids, toxic saponins, or hydro- 

 cyanic acid. 



URINE EXAMINATION. 



In order to determine what effect is produced in the urine following 

 the ingestion of H. hoopesii, a number of 24-hour samples of urine 

 from several sheep were examined chemically and microscopically. 

 It was found that the total volume of the urine was diminished, in 

 some cases enormously so. The urea excretion was also markedly 

 diminished, while the content of ammonium compounds was much 

 increased. Sugar was not found, but albumin frequently appeared, 

 especially after prolonged feeding. When the feeding of H. hoopesii 

 was discontinued the volume and urea content of the urine increased, 

 while the ammonia quickly fell to normal. These results indicate a 

 functional disturbance of the liver, since it is in this organ that the 

 conversion of ammonium compounds to urea is largely effected. The 



