Enzyme Changes within Muscle Fibers in Genetic and Nutritional Muscular Dystrophy
Summary and Conclusions Biopsy preparations of pectoral and gastrocnemius muscles from normal and genetic dystrophic chicks, and from chickens developing myopathy following diets deficient in vitamin E and sulfuramino acids, were examined histologically; serial sections were prepared to demonstrate...
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Veröffentlicht in: | Experimental biology and medicine (Maywood, N.J.) N.J.), 1968-11, Vol.129 (2), p.384-390 |
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Sprache: | eng |
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Zusammenfassung: | Summary and Conclusions
Biopsy preparations of pectoral and gastrocnemius muscles from normal and genetic dystrophic chicks, and from chickens developing myopathy following diets deficient in vitamin E and sulfuramino acids, were examined histologically; serial sections were prepared to demonstrate activity of several glycolytic and oxidative enzymes. Histological and histochemical characteristics of genetic and nutritional myopathies are similar in pectoral and gastrocnemius muscles, but more intense in the former. Coagulation necrosis attacks individual fibers or portions of fibers in the earlier stages of the disease. Before other histological alterations appear, white fibers enlarge and manifest the oxidative enzyme characteristics of red muscle fibers. Apparently, muscle fibers early in the myopathic process contain more enzymes, both oxidative and glycolytic, than do the normal muscle fiber. With the development within a muscle fiber of coagulation necrosis, reactions for both oxidative and glycolytic enzymes are diminished or completely absent. The early and extensive vulnerability of the pectoral muscle of chickens for dystrophic change is an index of its high white fiber content. With reference to enzyme activity in the muscle fibers undergoing myopathic changes, apparently two processes occur during the process: at first some enzymes are increased in amount; then when necrosis occurs, various enzymes examined in this study are lost from the damaged fibers. |
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ISSN: | 0037-9727 1535-3702 1535-3699 |
DOI: | 10.3181/00379727-129-33327 |