X. EFFECTS OK DEFICIENCY 265 



B. IN ANIMALS 



HENRY SHERMAN 



It is comparatively simple to iiulute vitamin Be deficiency symptoms in 

 animals; deficient synthetic diets and/or pyridoxin!* antaj^oiiists, such as 

 desoxypyridoxinc, have been employed for this purpose. A description of 

 the deficiency \'aries with the species of animal, hut there are a few genei'al 

 symptoms which appear to be common to most animals. The differences 

 among the animals appear to be in degree rather than in kind. In general, 

 N'itamin Be deficiency in animals induces retarded growth, several types of 

 anemia, epileptiform fits, and characteristic lesions of the skin. The vitamin 

 complex appears, therefore, to play an important role in blood, nerve, and 

 skin metabolism. 



1. Rats 



Poor weight gain is one of the earliest signs of a vitamin Be deficiency; 

 this is often apparent within five daj^s.^' ^ Accompanying this failure in 

 growth are usually a decrease in appetite and a marked interference in 

 efficiency of food utilization.^- ^ With this poor growth there is a reduction 

 in the size of the accessory organs of reproduction and deci-eased sexual 

 behaxnor.'" Simple omission of the vitamin has onl}' a slightly adverse 

 effect on reproduction." Howexer, the administration of desoxypyridoxinc 

 in the deficiency diet induces a high incidence of resorptions. The growth 

 of suckling young born from vitamin Be-deficient mothers is retarded 

 early in the lactation period, and survival to weaning is very rare. 



Vitamin Be avitaminosis induces a symmetrical dermatitis or acrodynia 

 in the peripheral areas of the body such as the tail, paws, nose, mouth, and 

 ears."*' ^-- ^^ Very often, this acrodynia is accompanied by an edema of the 

 corium and a scaliness of the extremities." This pathological condition was, 

 in fact, used as the basis of the first biological assay procedure. There have 

 been reports, however, that the acrodynia cannot be produced consistently 

 and that the \ntamin only modifies some of the dermal lesions.^^' '^ The 



' H. Sherman, Proc. Nutrition Sijjnposium Columbia Univ. School of Public Health' 

 p. 15 (1947). 



* H. Sherman, L. M. Campling, and R. S. Harris, Federation Proc. 9, 371 (1050). 



^ B. Sure and L. Easterling, J. Nutrition 39, 393 (1946). 

 '» G. A. Emerson and H. M. Evans, Am. J. Physiol. 129, 352 (1940). 

 " M. M. Nelson and H. M. Evans, /. Nutrition 43, 281 (1951). 

 "" E. E. Snell and A. N. Rannefeld, /. Biol. Chem. 157, 475 (1945). 

 •2 T. W. Birch, P. Gyorgy, and L. J. Harris, Biochcm. J. 29. 2830 (1935). 

 '3 P. Gyorgy and R. E. Eckhardt, Nature 144, 512 (1939). 

 '* W. Antopol and K. Unna, Proc. Sac. Exptl. Biol. Med. 42, 120 (1939). 

 's W. L. Dann, J. Biol. Chem. 128, XVIII (1939). 



