344 ASCORBIC ACID 



ported that anaphylactic shock in guinea pigs with partial vitamin C defi- 

 ciency is much more severe than it is in normal animals or than in animals 

 on the verge of scurvy. Bronfenbrenner et al.^^- studied experimental allergy 

 and its prevention in guinea pigs. They reported finding that ascorbic acid 

 has no influence on the development of sensitivity or prevention of shock, 

 once the animal is sensitive. They suggested that an animal on a diet 

 lacking vitamin C may develop alterations in the intestinal tract and, if 

 already sensitized parenterally, will as a consequence of the vitamin defi- 

 ciency develop an increased rate of absorption from the intestine, allowing 

 it to absorb the antigen more readily, resulting in shock resembling ana- 

 phylaxis produced parenterally. No histological evidence of such intestinal 

 alterations was presented, however. 



The fact that several other investigators have been unable to confirm 

 the finding that ascorbic acid reduces anaphylactic reactions in guinea pigs 

 indicates that the problem has not yet been satisfactorily solved.^^'"^^^ 



9. Reproduction 



Goettsch^^^ reported that female guinea pigs deprived of vitamin C main- 

 tained a regular estrus rhythm until they began to lose weight. If they 

 received an amount of the vitamin much less than sufficient to protect them 

 from chronic scurvy the cycles continued. Kramer et al.^^^ observed, how- 

 ever, that when females were kept on a vitamin C-free diet there were no 

 signs of estrus. Harman^^^ reported that males of comparable ages succumb 

 to the effects of ascorbic acid deficiency sooner than do females. They 

 became sexually inactive within 3 or 4 days after being put on an ascorbic 

 acid-free diet. The testes were found to leave the scrotum and to return 

 to the body. Normal spermatozoa were not produced, and the entire Avails 

 of the seminiferous tubules appeared to be degenerating. 



Ingier'* found that the susceptibility of the female to scurvy is greatly 

 increased during pregnancy although marked sjinptoms usually do not 

 develop until after parturition. Definite scurvy was produced in the fetus 

 as early as the tenth to fifteenth day after the diet of the mother had been 

 changed. The litters were frequently premature or stillborn and showed 

 retarded growth if vitamin C was lacking. Reyher et al}^^ confirmed Ingier's 



^82 J. Bronfenbrenner, D. M. Hetler, F. M. Love, and J. M. Burnett, /. Allergy 11, 



466 (1940). 

 «3 W. Scliafer, Z. Immunitatsforsch. 91, 394 (1937). 



«* J. Van Niekirk, Acta Brevia Neerl. Phijsiol. Pharmacol. Microbiol. 7, 144 (1937). 

 «" S. Raff el and R. R. Madison, J. Infectious Diseases 63, 71 (1938). 

 «" G. Walther, Z. ges. exptl. Med. 105, 584 (1939). 

 ^" P. Vallery-Radot, G. Mauric, and M. A. Holtzer, Cotnpt. rend. soc. bid. 136, 281 



(1942). 

 «8 M. Goettsch, Ain. J. Physiol. 95, 01 (1930). 

 «» P. Reyher, E. Walkhoff, and O. Walkhoff, Miinch. Med. Wochschr. 75, 2087 (1928). 



