IX. EFFECTS OF DEFICIENCY 651 



ketosteroid from the inner cortical zones (reticularis and fasciculata), ac- 

 companied and followed by progressive depletion of sudanophilic droplets 

 from the same area. Shortly thereafter, foci of necrosis and hemorrhage 

 appeared in these zones. This progressed in severe cases to almost total 

 destruction of the cortex, only a thin layer of intact cells remaining in the 

 zona glomerulosa. 



A number of laboratories have reported failure to observe the more ad- 

 vanced stages of adrenal damage, and some investigators have found no 

 pathological changes observable in gross or by microscopic examination. 

 Cowgill and coworkers" have obtained consistent, rapid, and marked 

 changes by using weanling rats from mothers placed on the deficient diet 

 immediately after birth of the offspring. 



Because of the fact that depletion of the lipoids of the adrenal cortex 

 preceded cortical necrosis and hemorrhage, it was proposed by Ashburn^ 

 that the adrenals of pantothenic acid-deficient rats might be functionally 

 insufficient. It had earlier been suggested by Morgan and Simms^ that the 

 graying and other physical changes of senescence, which they reported as 

 being associated with a deficiency of filtrate factor, might be mediated 

 through the adrenal. These investigators reported further that graying in 

 rats could be cured by relatively large doses of adrenal cortical extract^ 

 or by thyroid extract. ^^ These results have not been confirmed. ^^' ^^ In fur- 

 ther support of the concept of adrenal insufficiency in pantothenic acid 

 deficiency in rats are the results of Gaunt and coworkers, ^^ who demon- 

 strated a greater sensitivity of their animals to water intoxication. 



In opposition to the suggestions that the adrenal of the pantothenic acid- 

 deficient rat might be functionally insufficient, Deane and McKibbin^" pro- 

 posed that there might be overstimulation of the gland due to a stress re- 

 action. They presented cytological and physiological data in support of 

 this point of view. McQueeney et al}^ showed also that deficient animals on 

 drastically restricted sodium intake showed no defect in sodium conserva- 

 tion. Perry and coworkers'^ reported that pantothenic acid-deficient rats 

 showed no loss in ability to react to stress as judged by discharge of ascorbic 

 acid from the adrenal. Ershoff et al}^ presented evidence that there was no 



" G. R. Cowgill, R. W. Winters, R, B. Schultz, and W. A. Krehl, Intern. Rev. Vitamin 

 Research 23, 275 (1952). 



12 A. F. Morgan and H. D. Simms, J. Nutrition 19, 233 (1940). 



" C. W. Mushett and K. Unna, /. Nutrition 22, 565 (1941). 



" R. B. Schultz, Thesis, Yale University School of Medicine, 1952, quoted bj^ Cow- 

 gill et al. in ref. 11. 



16 R. Gaunt, M. Liling, and C. W. Mushett, Endocrinologij 38, 127 (1946). 



16 A. J. McQueeney, L. L. Ashburn, F. S. Daft, and R. R. Faulkner, Endocrinology 

 41, 441 (1947). 



" W. F. Perry, W. W. Hawkins, and G. R. Gumming, Am. J. Physiol. 172, 259 (1953). 



18 B. H. Ershoff, R. B. Alfin Slater, and J. G. Gaines, /. Nutrition 50, 299 (1953). 



