IV. BIOCHEMICAL SYSTEMS 223 



in teeth^' are also suspect, since it is well established that a deficiency of 

 vitamin A leads to marked degenerative changes in the dentine and enamel 

 of teeth;"- furthermore the histological changes observed in vitamin A defi- 

 ciency could not be cured by ascorbic acid, but only by vitamin A. 



The evidence would therefore suggest that the lowered ascorbic acid 

 content of tissues of vitamin A-deficient animals is due to inanition asso- 

 ciated with the deficiency rather than to any specific effect of vitamin A 

 on the synthesis of ascorbic acid. 



The synthesis of ascorbic acid in animals has also })een linked with 

 thiamine and riboflavin" • ^'* With both these deficiencies the ascorbic acid 

 content of the tissue of rats and mice has been shown to be low. The stimu- 

 lation of synthesis shown by a normal animal after chloretone treatment 

 was not observed in animals deficient in either thiamine or riboflavin. ^^ The 

 claim was made that these observations were directly due to a lack of these 

 essential nutrients and not due to inanition. The suggestion that ascorbic 

 acid may be synthesized in the narcotized animal from pyruvate and that 

 the process requires the participation of both thiamine and riboflavin is of 

 interest. 



5. Glucoascorbic Acid and Synthesis of Ascorbic Acid 



The report that a scorbutic-like condition in the rat, an animal which 

 normalh^ synthesizes its own ascorbic acid, could be induced by the admin- 

 istration of glucoascorbic acid,^^ an analog of ascorbic acid, did much to 

 enliven interest in this substance as a means of throwing more light on the 

 mechanism of the synthesis. Subsequent studies, however, have shown 

 that the symptoms produced by glucoascorbic acid are not identical with 

 those of scurvy ;^^ the condition cannot be cured by feeding ascorbic acid, 

 and there is no antagonism between these two substances w'hen judged 

 either by histological examination of teeth in guinea pigs or by the changes 

 in serum phosphatase." Glucoascorbic acid appears to produce toxic symp- 

 toms which are not due to any interference in the synthesis or functioning 

 of L-ascorbic acid but are due to the toxic action of the substance itself.^* 



'1 G. Jonnson, A. L. Obel, and K. Sjohcrg, Z. Vitaininforsch. 12, 300 (1942); 15, 115 

 (1945). 



" S. B. Wolbach and P. Howe, Aw. J. Pathol. 9, 275 (1933); P. Boyle, J. Dental Re- 

 search 13, 39 (1933); H. Mellanby, Brit. Dental J. 67, 187 (1939). 



" E. L. Kennaway and M. E. Daff, Brit. J. Exptl. Pathol. 27, 63 (1946). 



">* S. C. Roy, S. K. Roy, and B. C. Guha, Nature 158, 23S (1946). 



" D. W. Wolley and L. O. Krampitz, J. Exptl. Med. 78, 353 (1943). 



^8R. J. Gorlin, J. Dental Research 29, 208 (1950). 



" B. S. Gould, Arch. Biochem. 19, 1 (1948). 



" W. G. Shafer, J. Dental Research 29, 831 (1950). 



