514 THE TOCOPHEROLS 



week), the values were correlated with the fat content. Pasteurization 

 caused no loss. Evaporated cow's milk and whole milk powder contained 

 23 to 40 7 of tocopherol per gram of fat; proprietary infant foods, 29 to 

 171 7. 



VII. Effects of Deficiency 



KARL E. MASON 



A. IN ANIMALS 

 1. Introduction 

 a. General Considerations 



More than a quarter century has passed since the existence of vitamin E 

 (a-tocopherol) was definitely established. Its first recognized function as 

 an antisterility factor for the laboratory rat has been overshadowed by its 

 demonstrated need for maintenance of structural and functional integrity 

 of skeletal muscle, cardiac muscle, smooth muscle, and, in some animals, 

 the peripheral vascular system. Tocopherols play an important role as 

 intracellular antioxidants, related especially to the stabilization of ingested 

 fats and possibly of products arising in the metabolic synthesis and deg- 

 radation of lipids, and they may also function in a detoxifying capacity. 

 Morphologic alterations arising in the course of vitamin E deficiency may 

 well represent localized reactions of particularly susceptible tissues to loss 

 of these vital antioxidants or, secondarily, to dysfunction of enzyme sys- 

 tems in which tocopherols actively participate. 



The histopathologic lesions of vitamin E deficiency are remarkably 

 varied, they represent morphologic alterations in a number of unrelated 

 tissues, they seem not to be related to dysfunction of any specific type of 

 cell or tissue, and they are of such a nature that restoration of normal 

 morphology rarely occurs after tocopherol therapy, even though the physi- 

 ological or biochemical disturbances are corrected. Most lesions are de- 

 pendent upon fat in the diet, and their onset and intensity are accentuated 

 in proportion to the amount and degree of unsaturation of the fat used. 

 There are the possibilities that unsaturated fats destroy dietary traces of 

 the vitamin in the diet or the gut, that they or their oxidation products 

 produce a direct cell injury which is superimposed upon that due to lack 

 of vitamin E, and that excess utilization of tocopherols to stabilized un- 

 saturated fats being incorporated into cell lipids hastens depletion of tissue 

 tocopherols and the precipitation of deficiency manifestations (which may 

 or may not be related to lipid metabolism of the cells involved). Conceivably, 



