Experimentally Induced Selenium-Vitamin E Deficiency in Growing Swine: Selective Destruction of Type I Skeletal Muscle Fibers

SUMMARY In 2 experiments, 8 weanling, female pigs were fed a semisynthetic, torula yeast ration deficient in selenium (Se) and vitamin E (E). Six control pigs were fed Se-adequate rations and remained normal. Lesions of skeletal myodegeneration, mulberry heart disease (mhd), and hepatosis dietetica (hd) were produced in the pigs fed the Se-E-deficient ration. Onset and progression of the lesions were detected and assayed by sequential measurement of activity of several plasma enzymes; glutamic oxalacetic transaminase (got), creatine phosphokinase (cpk), alpha-hydroxy-butyric acid dehydrogenase (hbd), isocitric dehydrogenase (icd), and lactic dehydrogenase (ldh). Plasma enzymic activity hecame increased when the concentration of Se had decreased to 0.04 p.p.m. in the liver and 0.03 p.p.m. in muscle. Pigs fed the Se-E-deficient ration were killed at 3, 5, 6, 7, 12, 14, 18, and 21 days after the plasma enzymic activity was elevated. Serial sections of psoas muscle fibers were evaluated with enzyme histochemical procedures, including tests for myofibrillar adenosine triphosphatase (atp-ase), nicotinamide adenine dinucleotide (nad) diaphorase, and phosphorylase. Features common to all pigs fed the Se-E-deficient ration were selective destruction of type J skeletal muscle fibers and lack of phosphorylase activity in type II fibers. We believe this is the first description of nutritional myopathy in any animal species that resulted in such selective enzyme histochemical alterations.