556 THE TOCOPHEROLS 



body appears to represent the major site of tocopherol deposition and may 

 therefore best reflect the tocopherol status of the body as a whole. 



c. Histopathology 



The histopathologic lesions of experimentally induced deficiencies often 

 have a close counterpart in the corresponding deficiency state in man. This 

 is true of vitamin C and of vitamins A, D, and K, insofar as the period of in- 

 fancy and early childhood is concerned ; however, differences in responsive- 

 ness of the adult organism and the tenacity with which its tissues retain 

 traces of the fat-soluble vitamins seldom permit outspoken symptomatology 

 or histopathologic changes. It is notably difficult to induce manifestations 

 of vitamin E deficiency in mature animals that have built up considerable 

 stores of tocopherol. Furthermore, the fact that tocopherol storage is chiefly 

 in the adipose tissue, and thereby much less subject to interference by dis- 

 ease processes such as influence storage of vitamin A in the liver, may ex- 

 plain why there is so little evidence of vitamin E inadequacy in man other 

 than during early infancy, as discussed previously. 



Histopathologic approaches to the question of vitamin E deficiency in 

 man have been generally twofold. One is based upon the occurrence of an 

 acid-fast pigment commonly associated with the lesions of experimental 

 vitamin E deficiency; the other relates to striking similarities between the 

 muscle lesions of progressive muscular dystrophy in man and those common 

 to the various species of animal in which vitamin E deficiency has been 

 produced. 



(1) Acid-Fast Pigment (Ceroid). An acid-fast pigment, sometimes re- 

 ferred to as ceroid, occurs in the smooth and striated musculature and 

 becomes disseminated throughout the reticulo-endothelial system, after 

 prolonged vitamin E deficiency in certain animals; in organs such as the 

 sex glands and the adrenal, where small amounts of this pigment occur 

 normally, there may be a conspicuous increase. Excess of intracellular, 

 unsaturated lipids or fat peroxides and inadequacy of tocopherols as anti- 

 oxidants are considered primary factors in the genesis of this pigment. A 

 comparable pigment has been described by Wolf and Pappenheimer-"^ in 

 various parts of the central nervous system, and by Pappenheimer and 

 Victor^"** in a variety of other tissues and organs from routine autopsies. 

 They report that, in general, the occurrence of acid-fast pigment in human 

 tissues tends to be associated with hepatic cirrhosis and hemochromatosis, 

 celiac disease, pancreatic fibrosis, and non-tropical sprue, except for its 

 occasional location about focal degenerative lesions such as atheromatous 

 placques and areas of follicular atresia. It is of interest that acid-fast pig- 



207 A. Wolf and A. M. I'apponlieimer, J. Ncuropathol. Exptl. Neurol. 4, 402 (1945). 

 M8 A. M. Pappenheimer and J. Victor, Am. J. Pathol. 22, 395 (1946). 



