650 pantothenic acid 



1. Rats 



The signs of pantothenic acid deficiency observed in the rat are failure 

 of growth, achromotrichia (in black, hooded, or brown animals), dermatitis, 

 porphyrin staining of the fur and whiskers, "spectacled" eyes (circumocular 

 loss of hair), a characteristic spastic gait, closure of the eyes by a sticky 

 exudate, and, in some animals, an obvious anemia. At autopsy, the adrenals 

 may be enlarged, very dark red in color, and apparently engorged with 

 blood. This advanced stage of adrenal damage has not been observed in all 

 laboratories but when present, it presents a striking picture that cannot be 

 overlooked. There is a marked reduction of body fat. Histological examina- 

 tion has revealed lesions in skin, adrenal, thymus, bone marrow, testis, 

 intestine, bone, and kidney. In mature pantothenic acid-deficient rats, 

 reproduction is impaired. 



a. Adrenal Necrosis and Hemorrhage 



One of the most interesting and significant of these changes is a fatal 

 cortical necrosis and hemorrhage of the adrenal gland. ^' ^ Hyperemia and 

 hemorrhage in the adrenal cortex and medulla had been described earlier 

 as part of a panmyelophthisis syndrome due to an unknown deficiency,^ 

 and atrophy of the adrenal without mention of necrosis or hemorrhage had 

 also been described and attributed to filtrate factor deficiency.'* Daft et al} 

 demonstrated the effectiveness of pantothenic acid in the prevention or cor- 

 rection of the adrenal necrosis, hemorrhage, and other changes w^hich they 

 had observed, and these results have been repeatedly confirmed.^-'' Gross 

 and histological examinations of the adrenals have been made in several 

 laboratories.*'!" Grossly, the adrenals are swollen and dark. Ashburn^ de- 

 scribed the microscopic findings as congestion, hemorrhage, atrophy, ne- 

 crosis, scarring, fibrosis, hemosiderin deposition, and cortical fat depletion. 

 Deane and McKibbin^" studied the sequence of events in the development 

 of the adrenal lesions. The first changes noted were a disappearance of 



1 F. S. Daft and W. H. Sebrell, Public Health Repts. (U.S.) 54, 2247 (1939). 



2 F. S. Daft, W. H. Sebrell, S. H. Babcock, Jr., and T. H. Jukes, Public Health Repts. 

 (U.S.) 55, 1333 (1940). 



3 P. Gyorgy, H. Goldblatt, F. R. Miller, and R. P. Fulton, /. Exptl. Med. 66, 579 

 (1937). 



^ A. F. Morgan and H. D. Simms, Science 89, 565 (1939). 



s R. C. Mills, J. H. Shaw, C. A. Elvehjem, and P. H. Phillips, Proc. Soc. Exptl. Biol. 

 Med. 45, 482 (1940). 



« W. D. Salmon and R. W. Engel, Proc. Soc. Exptl. Biol. Med. 45, 621 (1940). 



^K. Unna, /. Nutrition 20, 565 (1940). 

 [8 A. A. Nelson, Public Health Repts. (U.S.) 54, 2250 (1939). 

 l^ L. L. Ashburn, Public Health Repts. (U.S.) 55, 1337 (1940). 

 '0 H. W. Deane and J. M. McKibbin, Endocrinologtj 38, 385 (1946). 



