240 ASCORBIC ACID 



and that enzymic activity was restored to normal on treatment with ascor- 

 bic acid. These results were substantiated for guinea pigs by several work- 

 gj.g 166-169 Scurvy is not the only disease, however, in which a decrease in 

 the phosphatase of the blood occurs; diseases in which there is a stoppage 

 of growth accompanied by loss of weight produce similar results. ^^^ How 

 far the reduction of phosphatase activity is related specifically to a defi- 

 ciency of L-ascorbic acid remains in doubt. Attempts to exclude the effect 

 of inanition were made with guinea pigs by means of the paired-feeding 

 technique, '^'^ but even under these conditions the scorbutic animals lost 

 more weight than their paired controls, and the greater decrease in the 

 phosphatase activity of the tissue of the scorbutic animals may have been 

 due to this cause. More recently^^" a further attempt has been made to 

 differentiate between inanition and cessation of growth on the one hand 

 and the effect of L-ascorbic acid on the other on the phosphatase activity 

 of both bone and serum. Evidence was obtained indicating that the fall in 

 the phosphatase content of the serum and in the zone of provisional calci- 

 fication of the costochondral junctions and the tibiae, observed during the 

 development of scurvy, is caused by the scorbutic condition, although in 

 the later stages the fall in weight may be a contributary factor. 



That L-ascorbic acid per se does not regulate the phosphatase content 

 of the tissue is seen from the fact that 18 hours after the intraperitoneal 

 injection of sufficient of the vitamin to saturate the tissues no rise in the 

 phosphatase activity of the tissues of scorbutic animals could be observed; 

 only after 2 days when the therapeutic action of the vitamin was well in 

 progress was the rise of the enzymic activity noted. Ascorbic acid does not, 

 therefore, appear to act directly on the enzyme, but rather indirectly 

 through restoring the scorbutic condition of the tissues to normal. Our 

 knowledge at present is not sufficient to indicate whether the phosphatase 

 activity characteristic of the scorbutic state results from an interference 

 in the synthesis of the enzyme or whether it is due to a transference of the 

 enzyme from some tissues to other tissues more affected l^y the deficiency. 

 The serum phosphatase is the first of the phosphatases to decrease during 

 the development of scurvy and the last to reach its normal level after cure, 

 which suggests that it may fulfill some protective function. The fall in the 

 phosphatase of bone may be due to a disturbance in the function of the 

 osteoblasts caused by local scorbutic lesions. It is possible, therefore, that 

 the low phosphatase content of bone may l)e due to poor synthesis, and 



i«6 G. Soz, C. Cattaneo, and M. C. Gabbrielli, Enzt/inologia 3, 29 (1937). 

 187 E. N. Todhunter and W. Brewer, Am. J. Physiol. 130, 310 (1940). 

 i«8 H. Schwachman and B. S. Gould, /. Nutrition 23, 271 (1942). 

 169 B. S. Gould and 11. Schwachman, /. Biol. Chern. 151, 439 (1943). 

 i7« H. R. Perkins and S. S. Zilva, Riochem. J., 47, 306 (1950). 



