VII. EFFECTS OF DEFICIENCY 517 



provide sources of vitamin E, combined with the presence of cod liver oil, 

 in cirrhosis-producing diets is the primary cause of ceroid production, and 

 that tocopherol supplements suppress or prevent its formation. Pigment 

 accumulation in adipose tissue in low-E rats'" (see p. 538), which provides 

 the closest morphologic counterpart to ceroid formation in the fatty in- 

 filtrated liver, is dependent upon the presence in the diet of fatty acids 

 having chain lengths of at least 18 carbon atoms and at least two unsatu- 

 rated bonds and is accentuated as chain length and unsaturation are in- 

 creased.^^ The presence of peroxides in the adipose tissue'- undoubtedly 

 plays a role in pigment formation. The evidence thus indicates that the 

 pigment of vitamin E deficiency and ceroid of nutritional cirrhosis are very 

 similar, if not identical. It should also be emphasized that this pigment 

 accumulates at the same sites and has much the same characteristics as 

 the so-called "wear and tear" pigment normally found to a limited extent 

 in the adrenal cortex, sex glands, and elsewhere in the body^' * For these 

 reasons care must be exercised in relating the occurrence of acid-fast pig- 

 ment to a state of avitaminosis E. 



2. Male Reproductive System 



o. Rats 



In male rats depleted of vitamin E from early life the seminiferous epi- 

 thelium shows no injury until active spermatogenesis begins, during the 

 third month of life, when a progressive and relatively rapid degeneration of 

 the epithelium occurs. Although there is close agreement among investiga- 

 tors regarding the distinctive character and irreparable nature of the histo- 

 pathologic changes,^^"'" there has been no satisfactory elucidation of the 

 underlying metabolic disturbances. The latter are so profound that vitamin 

 E therapy must be given 10 to 15 days prior to first appearance of histo- 

 logic injur}' in order to give full protection; therapy begun at intermediate 

 periods results in protection of certain seminiferous tubules but progressive 

 degeneration in others, or degeneration in all tubules, depending upon the 



i» K. E. Masou, H. Dam, and H. Granados, Anal. Record 94, 265 (1946). 



" L. J. Filer, Jr., R. E. Rumer\', andK. E. Mason, Trans. 1st Conf. on Biol. Antioxi- 

 dants, Josiah Macy, Jr. Foundation, New York, p. 67 (1946). 



'- H. Dam and H. Granados, Acta. Physiol. Scand. 10, 162 (1945). 



" K. E. Mason, /. Exptl. Zool. 45, 159 (1926); Am. J. Anat. 52, 153 (1933). 



'^ H. M. Evans and G. O. Burr, Mem. Univ. Calif. 8, 1 (1927). 



13 A. Juhdsz -Shaffer, Virchow's Arch. path. Anat. u. Physiol. 281, 3 (1931); 286, 834 

 (1932). 



'^ A. Ringsted, Dissertation, Undersogelser over testis' histoj)athologi ved E-avi- 

 taminose; en eksperimentel-morfologisk studie. Nj't Xordisk Forlag, Copen- 

 hagen, 1936. 



" C. Engel and L. H. Britschneider, Intern. Z. Vitaminforsch. 13, 58 (1943). 



