VII. EFFECTS OF DEFICIENCY 541 



c. Kidncij 



A progrossi\-o nephrosis of tlu' kidney occurs in lo\v-E rats, inxoix'inji; 

 isolated convoluted tubules of the outer cortex after 3 to 4 months of de- 

 ficiency and hecominj^ (juite generalized 1)}^ the tenth month.' The glomeruli 

 show little change, but the tulnilar epithelium becomes coarsely grainilar, 

 irregular in contour, and separated from the basement membrane to form 

 an amorphous pale-staining layer. In advanced stages, the loops of Ilenle 

 and even the collecting tubules are involved. It is surprising that the rats 

 can survive with such widespread nephron damage. Acid-fast pigment has 

 been observed in the tubular epithelium of the rat,"*' '" monkey ,^^ and mink*- 

 in the absence of the nephrotic changes just described. 



(/. Tooth Depigmentation 



Depigmentation of the maxillary incisors of the rat is recognized as a 

 common manifestation of vitamin E deficiency; mandibular incisors are 

 also involved if dietary protein is low.''*" This iron-containing, non-fluores- 

 cent pigment is continuously formed and deposited by the enamel organ 

 as the incisor is worn away by attrition. The depigmentation is secondary 

 to atrophic changes in the enamel organ. '^^' i'*^ According to Pindborg,'^* 

 there is edema and disorganization of the papillary layer, probably caused 

 by capillary damage in this region, followed by epithelial derangement and 

 cyst formation in the ameloblast layer. There is also a progressive deposi- 

 tion of acid-fast pigment in macrophages of the highly vascular periodontal 

 connective tissue. '"'^ After vitamin E therapy, function of the enamel organ 

 is restored and newly deposited enamel acquires its normal color. Depig- 

 mentation of maxillary incisors occurs also in the hamster,'^" but no histo- 

 pathologic studies ha\'e been reported. 



B. IN MAN 



1. General Considerations 



A state of avitaminosis E has not been shown to occur in man. There 

 are some similarities between certain manifestations of vitamin E defi- 

 ciency in experimental animals (such as fetal resportion, dystrophic changes 

 in skeletal muscle) and certain clinical disorders in man (habitual abortion, 

 progressive muscular dystrophy); yet, it has not l)een established that the 

 latter are either due to lack of vitamin K or l^enefited by therapeutic u.se of 

 the vitamin. On the other hand, there has arisen an extensive but decidedly 



"5 T. Moore, Biochem. J. 37, 112 (1943); Ann. N. Y. Acad. Sci. 52, 206 (1949). 



'^s J. T. Irving, Nature 150, 122 (1942). 



^" H. Granados, K. E. Mason, and H. Dam, ./. Dental Research 24, 197 (1945); 25, 



179 (1946). 

 '« J. J. Pindborg, J. Dental Research 29, 212 (1950); 31, 805 (1952). 



