VI. EFFECTS OF DEFICIENCY 229 



intestinal absorption of radioacti\'e calcium folloAving the administration of 

 A'itamin ]^ to ricketic rats. Shohl and Bennett^^ observed a decrease in 

 calcium retention, but at no time did the balance become negative in 

 ricketic pups. Phosphorus Avas still less positive in respect to the control 

 animals than was the calcium, and in some cases the phosphorus balance 

 was negative. The authors state that even on a diet high in phosphorus and 

 low in calcium the most marked deficiency lies in the phosphorus retention. 



7. Acidity of Intestinal Contents 



Zucker and Matzner^^ were the first to show that the pH of the feces of 

 rats becomes higher as the animals develop rickets, and falls again when 

 cod liver oil is fed. Similar results have been obtained with rats by Jephcott 

 and Bacharach'*" and Heller and Caskey.**^ 



Abrahamson and Miller,^- Yoder,^^ and Redman et al^^ observed a higher 

 pH of the intestinal contents of ricketic rats than in non-ricketic controls. 

 This difference appeared to be constant through the small and large in- 

 testines. When cod Yiver oil was given to the ricketic animals the hydrogen 

 ion concentration of the intestinal contents increased. Grayzel and Miller-'^ 

 have made similar observations on the dog, and Kline and associates'^ have 

 shown that irradiation of ricketic chicks decreases the pH of the proximal 

 part of the intestines but not of the distal portion. 



The significance of this change in acidity of feces and intestinal contents 

 and its relation to the cure of rickets is not clear at the present. According 

 to Sholil and Bing,*''' the change in acidity of feces did not occur when rats, 

 made ricketic on the Steenbock-Black diet, were cured by irradiation of the 

 food or by the addition of alkaline phosphates. Osei"** reports that the 

 effect of vitamin D on increasing the acidity of the intestinal contents and 

 feces of rats is inconsistent and non-specific, and Jones'*^ found that increas- 

 ing the acidity of the intestinal contents by other means did not cause a 



33 A. T. Shohl and H. B. Bennett, /. Biol. Chem. 76, 6.3.3 (1928). 



'9 T. F. Zucker and M. J. IMatzner, Proc. Soc. Exptl. Biol. Med. 21, 186 (1923-1924). 



*o H. Jephcott and A. L. Bacharaeh, Biochem. J. 20, 1.351 (1926). 



« V. G. Heller and C. Caskey, /. Nutrition 2, 59 (1929-1930). 



42 E. M. Abrahamson and E. G .Miller, .Jr., Proc. Soc. Exptl. Biol. Med. 22, 438 (1924- 



1925). 

 " L. Yoder, J. Biol. Chem. 74, .321 (1927). 



** T. Redman, S. G. Willimott, and F. Wokes, Biochem. J. 21, 589 (1927). 

 45 D. M. Grayzel and E. G. Miller, Jr., Proc. Soc. Exptl. Biol. Med. 24, 668 (1926- 



1927). 

 4«0. L. Kline, J. A. Kcoiian, C. A. Klvehjem, and E. B. Hart, ,/. Biol. Chem. 98, 



121 (19.32). 

 " A. T. Shohl and F. C. Biiig, ./. Biol. Chem. 79, 269 (1928). 

 « B. L. Oser, ./. Biol. Chem. 80, 487 (1928). 

 "J. H. Jones, /. Biol. Chem. 142, 557 (1942). 



