730 XI. VITAMINS E (tocopherols) 



("yelloAV fat disease" or "steatitis"). Harris et al.^^ suggest that the best 

 explanation for these phenomena is that the unsaturated dietary fats be- 

 come incorporated into adipose tissue cells which do not have enough 

 tocopherol to stabilize them or to counteract peroxide development; 

 polymerization takes place, or a combination with cell proteins, or both, to 

 produce acid-fast pigment. 



According to Jessen et al.,^^^ peroxidation of human adipose tissue occurs 

 in peripheral venous diseases in the case of vitamin E-deficient patients, as 

 demonstrated by the low but positive peroxide values. In ulcus cruris 

 (indolent ulcer of the leg), in which local changes in adipose tissue occur, 

 vitamin E exerts a beneficial effect, according to Burgess and Pritchard. ''•''' 

 For a further discussion of this pigment, the reader is referred to page 713. 



i. The Role of Vitamin E in Liver Cirrhosis. Most types of liver damage 

 are the result of the simultaneous operation of several factors, which may 

 or may not include vitamin E. Menschik and co-workers^ ^®'^^- reported 

 the occurrence of a pathologic condition in the liver of mice after fourteen 

 months on a high-fat diet low in vitamin E. Lipoproteic globules were 

 formed which were believed to result from abnormal metabolic changes 

 in the liv^er fat. 



In the case of nutritional cirrhosis, which can l)e produced readily in 

 rats fed diets lacking in the lipotropic factors, methionine or choline, the 

 usual pathologic changes are more severe when the deficient diet is com- 

 bined with a low vitamin E regimen. Under these conditions, the livers 

 become extremely browiiish yellow in color, and accumulations of ceroid 

 pigment can be observed in the cells, on histologic examination. '''^■^^^•^■^'' 

 This pigment appears to be the same as the acid-fast pigment laid down in 

 many tissues on a diet low in vitamin E. Although the tocopherols do not 

 influence the fibrotic changes which result from the lack of lipotropic 

 agents, they do retard or entirely prevent ceroid formation.'*'** Highly 

 unsaturated dietary fats accentuate the severity of the al)normality.''^^ 



A third type of liver injury involves a deficiency of vitamin E combined 

 with a low cystine intake and a deficiency of the so-called "Factor 3."^'''' 

 This abnormality occurs on certain diets low in vitamin E and lacking in 



3^" K. E. Jessen, J. Glavind, S. Hartmann, and H. Dam, Acta Pathol. Microbiol. Scand., 

 g£>, 73-76(1951). 



»i J. F. Burgess and J. E. Pritchard, /. Canad. Med. Ass c, 59, 242-247 (1948). 



»" Z. Menschik and T. J. Szczesniak, Anat. Record, 103, 349-363 (1949). 



^3 P. Gvorgy, Am. J. Clin. Pathol, 14, 67-88 (1944). 



3" H. Popper, P. Gvorgy, and H. Goldblatt, Arch. Pathol., 37, 161-168 (1944). 



^"•^ M. Wachstein, Proc' Soc. Exptl. Biol. Med., 59, I'i-ll (1945). 



'56 K. Schwarz, Proc. Soc. Exptl. Biol. Med., 77, 818-823 (1951); 78, 852-856 (1951). 



