VITAMIN E 341 



ether extracts of yellow corn, wheat embryo, and wheat seed, and in 

 commercial cottonseed and olive oils, but not in commercial coconut, 

 linseed, or sesame oils. Evans and Burr had also noted the relatively 

 low content of E in coconut oil. Sure (1927) also reported the presence 

 of vitamin E in appreciable amounts in butter fat, but stated that when 

 butterfat was fed to the extent of 10 per cent of the ration the results 

 were not as good as with 1 per cent of wheat oil as the source of 

 vitamin E. 



Shortly after the publication of the Memoir in which their work 

 on vitamin E up to that time had been summarized, Evans and Burr 

 (1927a) announced a new basal vitamin-E-free diet dispensing with 

 lard and using sucrose in place of starch. The diet consists of casein 

 prepared by the Van Slyke method 50, sucrose crystallized from 80 

 per cent alcohol 150, and a salt mixture (185) 8 parts, with distilled 

 water ad libitum containing a trace of potassium iodide, cod-liver oil 

 from 2 to 3 drops daily, and yeast from 700 to 1,000 milligrams daily. 



More recently Waddell and Steenbock ( 1928) have reported that a 

 ration composed of natural and varied food materials such as the 

 Steenbock (1923) stock ration can be completely freed from vitamin 

 E without affecting the vitamin A content of the ration by simple treat- 

 ment with ferric chloride in the proportion of 1 part to 99 of the ration. 

 The treatment consists in dissolving the correct proportion of the ferric 

 chloride in ether with a small amount of water, pouring the solution 

 over the ration and allowing the ether to evaporate. It is stated that 

 complete sterility is secured in the first gestation on this ration. 



Relation to Metabolic Processes 



Although it is beyond the scope of this monograph to discuss in 

 detail the characteristic histopathology of animals suffering from vita- 

 min E deficiency, for excellent discussion of which the reader is re- 

 ferred to Evans and Burr (1927d) and to Mason (1925), attention is 

 called to the different effects produced by lack of vitamin E upon the 

 male and female reproductive organs. As stated early in the chapter, 

 in the female there is no failure of ovarial but only of placental function. 

 In the male, however, the testes, while at first not adversely affected, 

 ultimately rather completely degenerate. Female sterility can always 

 be cured, since only temporary tissues are damaged, while male sterility 

 tends to go beyond recall through the breaking down of the permanent 

 testicular tissues. In attempting to explain these differences, Evans 

 suggests that both ovary and testis are originally equally favored with 

 the substance, but that the immensely greater cell production occurring 



