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  • Title: [Abnormalities in mitochondrial creatine kinase activity in cardiomyopathic hamsters].
    Author: Matsuo H.
    Journal: Hokkaido Igaku Zasshi; 1991 May; 66(3):348-55. PubMed ID: 1885160.
    Abstract:
    The creatine kinase system is related to intracellular high-energy phosphate transfer. Mitochondrial creatine kinase catalyzes the transfer of high-energy phosphate between creatine and ATP generated in mitochondria. Creatine phosphate generated in this process is transferred to myofibril. Mitochondrial creatine kinase abnormalities cause the decrease of ATP level in cytoplasm through the disorder of ATP transfer. If such decrease happens in myocardium the depressed cardiac function is suspected. I studied the time course of alterations of the creatine kinase system in BIO14.6 (the model of hypertrophic cardiomyopathy) at 5 weeks, 20 weeks, 50 weeks, and 62 weeks of age, and in BIO53.58 (the model of dilated cardiomyopathy) at 5 weeks and 20 weeks of age. In BIO14.6, creatine kinase activity of myocardium and isolated mitochondria was decreased in 20, 50, 62-week-old hamsters. The share of mitochondrial creatine kinase in the total tissue enzyme activity was decreased, and the share of BB form was increased in 50, 62-week-old hamsters. In BIO53.58, creatine kinase activity of myocardium and isolated mitochondria was decreased in 20-week-old hamsters. The share of mitochondrial creatine kinase was increased, and BB form was decreased in 5, 20-week-old hamsters. The experiments suggest alterations in the creatine kinase system occur at 20 weeks of age in BIO14.6 and at neonatal phase in BIO53.58. These alterations of creatine kinase system may contribute to depressed cardiac function in cardiomyopathy.
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