Human muscular dystrophy is a condition of unknown etiology which produces progressive and severe dysfunction of symmetrical groups of skeletal muscle. Although its clinical manifestations1-3 and patterns of heredity4-6 have long been recognized, relatively little attention has been given the study of distribution and utilization of metal ions in this disorder. In recent years, new impetus has been given the study of metal ions in health and disease by the increasing recognition of their important influences upon activities of enzymes. In muscular dystrophy, abnormal activities of various glycogenolytic enzymes,7-9 transaminase,10 nucleotidase,11 and creatine phosphokinase12 have been described. It is well known that all of the enzymes which catalyze the transfer of phosphate from adenosine triphosphate (ATP) to a phosphate receptor, or from a phosphorylated compound to adenosine diphosphate, (ADP) are activated by magnesium. Since ATP is necessary in such diverse functions as muscle contraction;
SMITH HL, FISCHER RL, ETTELDORF JN. Magnesium and Calcium in Human Muscular Dystrophy: Complexometric Analyses of Serum and Serum Ultrafiltrates. Am J Dis Child. 1962;103(6):771–776. doi:10.1001/archpedi.1962.02080020788006
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