568 NIACIN 



However, more recent studies using purified diets more adequately supplied 

 with vitamins have shown findings generally similar to the observations 

 already reported. 2- ^^^ 



3. Rats 



Most investigators have observed little pathology in nicotinic acid- 

 deficient rats except retarded growth and non-specific deficiency signs such 

 as rough hair coat, porphyrin-caked whiskers and, occasionally, alope- 

 gjg^_26,27 Animals allowed to eat a nicotinic acid-deficient ration ad lib 

 voluntarily restrict their food intake and may thereby protect themselves 

 to some extent. Spector and associates'^' '^ force-fed a diet severely deficient 

 in both nicotinic acid and tryptophan to rats and observed striking pathol- 

 ogy. Alopecia, bloating, diarrhea, hunchback, jumping, screeching, convul- 

 sions, mild anemia, kidney enlargement, degeneration of the testes, fatty 

 infiltration of the liver, atrophy and degeneration of visceral and cardiac 

 muscle, and keratinization of the cornea were observed. Most of these 

 abnormalities were undoubtedly due primarily to tryptophan deficiency 

 rather than nicotinic acid. The addition of nicotinic acid in the absence of 

 added tryptophan was without any substantial effect on the deficiency 

 syndrome. Nicotinic acid can protect to some extent against congenital 

 cataract m rats when the diet contains marginal amounts of tryptophan 

 as shown by Pike.^" The stomach of deficient rats is normal to gross in- 

 spection, and acid-pepsin secretion is normal. ^^ However, Bourne^- found 

 that the gastric mucosa was reduced in thickness, mainly at the expense of 

 the oxyntic cells. Only slight degenerative changes were noted in the rest 

 of the gastrointestinal tract. Johnston and Weitz,^^ on the other hand, 

 found marked degenerative changes in the Golgi apparatus in the columnar 

 absorbing cells of the duodenum in nicotinic acid-deficient rats. Bourne^' 

 also noted loss of staining ability and decrease in number of acidophile cells 



22 G. E. Cartwright, B. Tatting, and M. M. Wintrobe, Arch. Biochem. 19, 109 (1948). 



23 M. M. Wintrobe, H. J. Stein, R. H. FoUis, Jr., and S. Humphreys, /. Nutrition 30, 

 395 (1945). 



2^ W. C. Powick, N. R. Ellis, L. L. Madsen, and C. N. Dale, J. Animal Sci. 6, 310 

 (1947). 



25 W. Burroughs, B. H. Edgington, W. L. Robinson, and R. M. Bethke, /. Nutrition 

 41, 51 (1950). 



26 W. A. Krehl, P. S. Sarma, L. J. Teply, and C. A. Elvehjem, J. Nutrition 31, 85 

 (1946). 



27 W. A. Krehl, L. J. Teply, and C. A. Elvehjem, Science 101, 283 (1945). 



28 H. Spector, J. Biol. Chem. 173, 659 (1948). 



29 H. Spector and F. B. Adamstone, /. Nutrition 40, 213 (1950). 

 3» R. L. Pike, J. Nutrition 44, 191 (1951). 



31 E. A. Hawk and J. M. Hundley, Proc. Soc. Exptl. Biol. Med. 78, 318 (1951). 



32 G. H. Bourne, Brit. J. Nutrition 4, xvi (1950). 



33 P. M. Johnston and E. M. Weitz, J. Morphol. 91, 79 (1952). 



