722 XI. viTAMixR E (tocopherols) 



a'. The Involvement of the Nervous System in Chronic Muscular Dys- 

 trophy: Most authorities agree that the dystrophic muscle lesions are of 

 myogenic rather than neurogenic origin. The early onset of the symptoms, 

 their biochemical nature, and their ready response to vitamin E therapy, 

 reported by Houchin and Mattill,*^^'^^" lend support to this conclusion. 

 However, in the case of the adult rat kept for some months on a low- 

 vitamin E diet, Eiiiarson and Ringsted'-'^- obser^-ed lesions in the dorsal 

 columns, dorsal nerve roots, and ventral horns of the spinal cord which, 

 they state, may partly account for the muscular changes. Monnier-^^--^^ 

 is in agreement with this \aewpoint. Lutti'ell and Mason-^^ and Malamud 

 et al.-^^ confirmed the demyelinization and gliosis in the posterior columns 

 and dorsal nerve roots, but not the changes in the ventral horn and py- 

 ramidal tracts. 



Telford -^^ noted a loss of motor and plastics, in the case of young rats, 

 secondary to degeneration of the muscle fibers. On the other hand, these 

 structures and the peripheral nerves have been reported to be normal in 

 nutritional myodegeneration of ducklings,-'^- guinea pigs,-^^--^* and young 

 rats.28« 



b' . Changes in Muscle Enzyme Systems in Chronic Muscular Dystrophy : 

 Since tocopherols are believed to act in general as inhibitors in most 

 enzyme systems, it is easy to explain why an increased rate of succinic acid 

 oxidation occurs in dystrophic hamster muscle, as showm by Houchin. ^^^ 

 On the other hand, the succinic dehydrogenase system is apparently un- 

 affected under the same conditions. '^^ Although there are general dis- 

 turbances in the phosphorylation mechanism in muscular dystrophy, as 

 reflected by a decreased creatine leveP^"*'^*^ and a reduction in adenosine 

 triphosphatase activity, ^^^ Rabino\atz and Boyer^^^ did not find any de- 

 crease in the level of oxidative phosphorylation of heart muscle of dystro- 

 phic rabbits. In the absence of vitamin E, cholinesterase is decreased m 

 liver, brain and serum. ^^^ 



2" C. N. Luttrell and K. E. Mason, Ann. Nexo York Acad. Set., 52, 113-120 (1949). 



280 N. Malamud, M. M. Nelson, and H. M. Evans, Ann. New York Acad. Set., 52, 135- 

 138 (1949). 



281 I. R. Telford, Anat. Record, 81, 171-181 (1941). 



282 A. M. Pappenheimer, M. Goettsch, and E. Jungherr, Storrs Agr. Expt. Sta. Bull. 229 

 (1939); Chern. Abst., 33, 9374 (1939). 



283 W. M. Rogers, A. M. Pappenheimer, and M. Goettsch, ./. Exptl. Med., 54, 167-169 

 (1931). 



28'» H. Chor and R. E. Dolkart, Arch. Pathol, 27, 497-509 (1939). 



286 M. Goettsch and E. F. Brown, /. Biol. Chem., 97, 549-561 (1932). 



286 J. P. Hummel, /. Biol. Chem., 172, 421-429 (1948). 



28T M. Rabinovitz and P. D. Boyer, Proc. Soc. Exptl. Biol. Med., 77, 103-105 (1951). 



288 H. Bloch, Helv. Chim. Acta, 25, 793-797 (1942). 



