Abstract
Rabbits were fed a vitamin E-deficient diet for 7 weeks. Control rabbits, paired for weight, were pair-fed an identical diet supplemented with vitamin E. After 3 weeks the expermental animals showed a rise in serum creatin kinase activity which was attributable to the muscle isoenzyme (MM). No rise in creatine kinase activity or appearance of MM was noted in the serum of the control rabbits. Total creatine kinase activity and MM activity were reduced in the gastrocnemii of the experimental animals while the activities of the brain (BB) and hybird (MB) isoenzymes were increased. The specific activity of BB based on immunochemically determined BB protein was not different from normal in either the experimental or control group. Activation of pre-existing inactive BB is probably not the explanation for increased BB activity in the gastroncnemii of the experimental group.
Highlights
Rabbits were fed a vitamin E-deficient diet for 7 weeks
After 3 weeks the experimental animals showed a rise in serum creatine kinase activity which was attributable to the muscle isoenzyme (MM)
Rio rise in creatine kinase activity or appearance of MM was noted in the serum of the control rabbits
Summary
(Received for publication, June 14, 1976, and in revised form, December 16, 1976). Diuision, Research Institute, The Hospital for Sick Children, Institute, Montreal, Canada. After 3 weeks the experimental animals showed a rise in serum creatine kinase activity which was attributable to the muscle isoenzyme (MM). Rio rise in creatine kinase activity or appearance of MM was noted in the serum of the control rabbits. The etiology and pathogenesis of the dystrophy are unknown but the rise in serum creatine kinase activity appears to be a sensitive indicator of the onset of the disease (2). It is not known which isoenzymes of creatine kinase are responsible for the elevated serum creatine kinase activity.’.
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