530 THE TOCOPHEROLS 



An important recent de^'elopment is the demonstration that ct-tocoph- 

 erylhydroquinone, which is a potent anticlystrophy compoiuid, has no 

 antisterihty activity^^'^' '' and undergoes little or no conversion to a-tocoph- 

 erol in vivoP^ Another oxidation product of tocophen'ol, a-tocopheryl- 

 quinone, is also antidystrophic but appears to have no antisterihty activity. 

 Thus a-tocopherol, the antisterihty vitamin, may represent a provitamin 

 for other compounds functioning as antidystrophy vitamins. An excellent 

 discussion of these and other aspects of experimental muscular dystrophy 

 has been presented by Mackenzie.^^'' 



b. Cardiac Muscle 



Hyaline necrosis and replacement fibrosis of carchac muscle, closely re- 

 sembling the changes occurring in skeletal muscle, have been observed in 

 the vitamin E-deficient rabbit,''^''' ^^' ^^ guinea pig, ^^''- ^^ young calf,^''^- ^- <= 

 cow,^^' ^^ sheep, ^^' *^ goat,^^'' rat,"*' ^°-^- mouse,-^ hamster,-^ and cotton rat.-^ 

 The lesions are rapid in onset in herbivorous animals (rabbit, guinea pig, 

 sheep, and cattle), not associated with acid-fast pigment, and freciuently 

 the cause of sudden death through myocardial failure. This is in strik- 

 ing contrast to other laboratory animals (rat, hamster, and cotton rat) 

 in which extensive focal necrosis and scarring of the myocardium, with 

 accumulation of pigment in muscle fibers and macrophages, may exist 

 for many months without serious effects. Electrocardiographic changes of 

 varying degrees, indicati\'e of myocardial damage without involvement of 

 the conducting system (Purkinje fibers), have been found in the rat, guinea 

 pig, rabbit, cattle, and monkey. The most dramatic picture is seen in sudden 

 collapse of cattle in cardiac failure, usually with little or no symptomatology 

 prior to exitus.'*^ The phenomenon in the rabbit has received the 

 most thorough study, largely through the careful studies of Gatz and 

 Houchin,^^ who provide an excellent description of the electrocardiographic 

 and histopathologic changes. They believe that a phase of increased muscle 

 metabolism, as reflected in increased O2 consumption similar to that in 



83'' A. Issidorides and H. A. Mattill, J. Biol. Cheiu. 188, 313 (1951). 



83b J. B. Mackenzie and C. G. Mackenzie, Proc. Soc. Exptl. Biol. Med. 84, 388 (1953). 



83<= C. G. Mackenzie, In Symposium on N uirition, Johns Hopkins Press, Baltimore 



(1953). 

 8* A. J. Gatz and O. B. Houchin, Anat. Record 110, 249 (1951). 

 86 J. H. Bragdon and H. D. Levine, Am. J. Pathol. 25, 265 (1949). 

 88 S. Americano Freire and B. Figueiredo Magalhaes, Rev. brasil. biol. 3, 91 (.1943). 

 8' T. W. Gullickson and C. E. Calverley, Science 104, 312 (1946). 



88 T. W. Gullickson, Ann. N. Y. Acad. Sci. 52, 256 (1949). 



89 R. Culik, F. A. Bacigalupo, F. Thorj), Jr., R. W. Luecke, and R. H. Nelson, J. 

 Animal Sci. 10, 1006 (1951). 



90 S. Americano Freire, Brasil-med. 55, 308 (1941). 



91 G. J. Martin and F. B. Faust, Exptl. Med. and Surg. 5, 405 (1947). 



92 W. Ruppel, Arch, exptl. Pathol. Pharmakol. 206, 584 (1949). 



