Nil. KFFECTS OF DEFKIKNCY 525 



farm coiulitions aiul scorn undoubtedly duo to inadociuacy of vitamin E 

 in early life, closely resemi)les the early paralysis of lal)oratory mammals; 

 the same is true of muscle changes observed in puppies,^'" mink,^- ducks,^^ 

 i;oats,^'*-' and chicks'^' (where definato lesions have been observed only 

 in the pectoral muscles), and guppy fish.^^ Of particular interest are the 

 classic studios of Blaxter and coworkers, ^""^ who describe in detail the 

 symptomatology, gross pathology, biochemical alterations, and histo- 

 pathology of a muscular dystrophy produced in Ayrshire calves reared on 

 a low-E diet. The syndrome is indistinguishable from the long recognized 

 "white muscle" disease of calves. Dietary cod liver oil accentuated the 

 muscle lesions and alst) nullified otherwise protective doses of a-tocopherol, 

 as is also true of other hor))ivorous animals (guinea pig, rabbit, goat). 

 They describe swelling of muscle fibers, fragmentation, evidence of increased 

 breakdown or impaired synthesis of muscle globulins, and massive sarcolcm- 

 mic proliferation which they think reflects an attempt to maintain con- 

 stant the volume of the dystrophic muscle; it is their opinion that in differ- 

 ent species the latter is accomplished by varying degrees of sarcolommic 

 proliferation and fatty infiltration, thus accounting for much of the species 

 variation in general character of the muscle lesions observed. 



For a more detailed review and discussion of vitamin E as it applies 

 to the nutrition of farm and laboratorj^ animals, the reader is referred to 

 the recent review b\' Blaxter and Brown. ^^^ 



(2) Dystrophy in Rabbit and Guinea Pig. Herbi\-orous animals as a whole 

 appear to be particularly susceptible to withdrawal of vitamin E, and also 

 to the presence of unsaturated fats in the diet.''^"' ^" It was in the guinea 

 pig and rabbit that nutritional muscular dystrophy was first experimentally 

 produced by Goettsch and Papponheimer,''*^ although its relationship to lack 



^''' H. D. Anderson, C. .\. Elvehjem, and J. E. Gonce, Jr., Proc. Soc. Exptl. Biol. 



Med. 42, 750 (1939). 

 «2 K. ]•:. Mason and G. R. Hartsough, ./. Am. Vet. Med. Assoc. 119, 72 (1951). 

 " A. M. Pappenheimer and M. Goettsch, /. Exptl. Med. 69, 35 (1934). 

 "' L. L. Madsen, C. M. McCay, and L. A. Maynard, Proc. Soc. Exptl. Biol. Med. 30, 



1434 (1933); Cornell Univ. Agr. Expt. Sta. Mem. 178, 3 (1935). 

 ^^ H. Dam, I. Prange, and E. Sondergaard, Acta Pathol. Microbiol. Scand. 31, 172 



(1952). 

 «•>« K. L. Blaxter, P. S. Watts and W. A. Wood, Brit. J. Xntrition 6, 125 (1952). 

 «^bK. L. Blaxter and W. A. Wood, Brit. J. Nutrition 6, 144 (1952). 

 ^"= A. M. Mac.lonald, K. L. Blaxter, P. S. Watts, and W. A. Wood, Brit. J. Nutrition 



6, 164 (19.52). 

 «"^ K. L. Blaxter, W. A. Wood, and A. .M. .MaeDonald. Bnt. J. Nutrition 7, 34 (1953). 

 «"= K. L. Blaxter, F. Brown, and A. M. MacDonald, Brit. J. Nutrition 7, 105 (1953). 

 ^" K. L. Blaxter and F. Brown. Nutrition Abstr. & Rev. 22, 1 (1952). 

 « L. L. Madsoii, ./. Nutrition 11, 471 (19.36). 

 "^M. Goettsch and A. M. Pappenheimer, ./. Exptl. .Med. 54, 145 (1931). 



