X. EFFECTS OF DEFICIENCY 271 



protein diet favored the storage of the vitamin. Mice on deflciont diets often 

 develop fatty livers.^* This condition appeared more rapidly on a high 

 casein diet than on a low one. The addition of tryptophan to the deficient 

 diet hastened fatty liver formation. 



Silberherg and Levy®^ demonstrated that, in young mice deprived of 

 pyrido.xinc, cartilage growth and bone formation were inhibited; a high 

 protein diet accentuated this effect. Interdental bone growth ceased after 

 2 weeks, and recessive changes progressed in all periodontal structures." 

 The mandibular condyle showed slight narrowing of the cartilage cap 

 after 1 week. 



Young Swiss mice which had been fed a special vitamin Be-deficient diet 

 and given an injection of desoxypyridoxine developed granulocytosis and 

 lymphopenia.*^ In leukemic mice of the Ak strain, the deficiency augmented 

 the leukemic granulocytosis and shortened the survival time. 



There was a marked regression of lymphosarcoma implants in deficient 

 mice.®^ Tumor implants failed to develop in mice deprived of vitamin Be 

 prior to the inoculation. 



3. Hamsters 



Routh and Houchin^" reported that on a vitamin Be-deficient diet the 

 Syrian hamster developed an "acrodynia-like" dermatitis around the 

 mouth, lost weight, and died within 24 days. 



Shwartzman and Strauss" have produced a vitamin Be deficiency in the 

 male Syrian hamster. It was characterized by arrest of growth, diminished 

 food and water intake, progressive malnutrition, muscular weakness, and 

 changes of the fur. Increased amounts of xanthurenic acid were excreted 

 in the urine. Deficient animals died in 12 to 13 weeks. There were no cu- 

 taneous changes comparable to the classical "rat acrodynia." Epileptiform 

 seizures did not occur in the pyridoxine-deficient hamster, but there were 

 other symptoms of nervous disorder, such as an ataxic gait, or paresis of 

 one extremity, and priapism. Autopsy revealed a loss of fat tissue and 

 atrophy of lymphoid tissues, especially the thymus. The transamination 

 rate of heart muscle of pyridoxine-deficient hamsters was 30 to 40 % lower 

 than that of control animals fed ad libitum or restricted amounts of food; 

 succinoxidase acti\'ity was comparable to that of control animals.'- 



8« R. Silberherg and H. M. Levy, Proc. Sue. Exptl. Biol. Mai. 67, 259 (1948). 



«^ B. M. Levy, /. Dental Research 29, 349 (1950). 



«8 D. R. Weir, R. W. Heinle, and A. D. Welch, I'mc. Soc. Exptl. Biol. Med. 72, 457 



(1949). 

 «9 H. C. Stoerk, J. Biol. Chen. 171, 4.37 (1947). 

 '» J. I. Routh and O. B. Ilouchin, Federation Proe. 1, 191 (1942). 

 ■' G. Shwartzman and L. Strauss, ,/. Nutrition 38, 131 (1949). 

 '= G. Shwartzman and II. Hift, J. Nutrition 44, 575 (1951). 



