324 ASCORBIC ACID 



ity to synthesize vitamin C.^-^ Manganese, however, is not involved in the 

 synthesis of ascorbic acid in either the rat^^^ or the guinea pig.^-^ The injec- 

 tion of manganese into scorbutic guinea pigs resulted in no change in blood 

 phosphatase levels or in concentration of indophenol-reducing substances 

 in the liver. 



(G) Copper. Lindow et aL""^ stated that copper is present in all biological 

 fluids in a con(;entration sufficient to produce a rapid oxidation of the 

 vitamin C. It is known, however, that copper does not oxidize all the vita- 

 min C, owing to various protective mechanisms. De Caro^'*'' reported that 

 excessive amounts of copper induce a higher demand for ascorbic acid in 

 guinea pigs. However, Lesne et al.^^^ investigated the role of copper in the 

 utilization of ascorbic acid l)y the guinea pig and reported that addition of 

 copper to a scorbutigenic diet prevented the development of symptoms of 

 scurvy in the bones and joints and also caused these symptoms to recede 

 if supplementation with copper was not l)egun until after the symptoms 

 appeared. The animals receiving copper all lost weight, however, and none 

 of them survived beyond the fifty-sixth day. These results are of consider- 

 able interest, l)ut confirmatory^ e^ddence has not been reported. Hochberg 

 et alF^ conducted tests with human subjects to determine the effect of 

 copper ingestion (7 mg.) on the fate of dietary ascorbic acid (200 mg. daily) 

 and found no greater destruction as a result of the presence of the copper. 

 The effect of prolonged ingestion of copper on the excretion of the vitamin 

 was not determined. It is possible that under the conditions of these tests 

 the reserves of copper in the body were sufficient to supply the small 

 amounts needed for the catalytic oxidation of ascorbic acid since in the 

 presence of ascorbic acid there tends to be a continuous regeneration of the 

 catalyst. Amounts of copper in excess of this requirement would, therefore, 

 not be expected to have noticeable effects on the rate of oxidation of the 

 vitamin. 



e. Effect on Other Vitamins 



(1) Vitamin A. (a) Effect of Ascorbic Acid on the Level and Function 

 of Vitamin A. Kimble and Gordon^^* in studies with human subjects ob- 

 served that administration of ascorbic acid caused an increase in the blood 



326 W. F. Von Oettiiigen, Physiol. Revs. 15, 175 (1935). 



"^s M. N. Rudia, Nature 144, SG8 (1939). 



3" P. D. Boyer, J. H. Shaw, miuI P. II. Phillips, ./. Biol. Chon. 143, 417 (1942). 



328 J. T. Skinner and J. S. McIIargue, Am. J. Physiol. 145, 5G6 (1946). 



329 C. W. Lindow, C. A. Elvehjem, and W. H. Peterson, J. Biol. Chem. 82, 465 (1929). 



330 L. De Caro, Boll. soc. ital. hiol. sper. 13, 727 (1938). 



331 E. Lesne, M. Polonovski, and S. Briskas, Compt. rend. 217, 406 (1943). 



332 M. Hochberg, D. xMelnick, and B. L. Oser, ./. Xutrition 30, 225 (1945). 

 "3 M. Kimble and E. S. Gordon, ./. Biol. Chem. 128, Hi (1939). 



