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  • Muscular dystrophy  (3)
  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 315 (1980), S. 77-82 
    ISSN: 1432-1912
    Schlagwort(e): Muscle ; Lysosomes ; Calcium ; Muscular dystrophy
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary 1. The possibility that rapid Ca2+-uptake by skeletal muscle mitochondria may cause local reductions in pH i (by H+/Ca2+ exchange) and so promote lysosomal breakdown has been explored using amphibian and mammalian preparations. Recent studies suggested that such a sequence of events is possible in cardiac muscle. 2. However, extensive muscle damage can still be initiated in skeletal muscle when the mitochondria are uncoupled so that Ca2+-uptake is prevented. 3. DNP alone induces extensive myofilament degradation which is similar to that produced by A 23187 and caffeine and described previously. 4. It is suggested that (a) the known action of DNP in promoting lysosomal labilization in living cells is produced by mitochondrial uncoupling and the release of stored Ca2+, (b) raised [Ca2+] i promotes lysosomal breakdown in skeletal muscle, so that the hydrolases released effect myofilament dissolution rapidly. 5. DNP also rapidly causes septation and division of the mitochondria in mammalian skeletal muscle.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 305 (1978), S. 159-166 
    ISSN: 1432-1912
    Schlagwort(e): Caffeine ; Muscle ; Muscular dystrophy ; Calcium ; A23187
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary 1. Caffeine at concentrations above 5 mM was shown to cause rapidly extensive ultrastructural damage to the myofibrils of frog skeletal muscle. 2. The effect was promoted at lower temperatures, whereas the myofibrils were protected by prior exposure to procaine. 3. It is argued that caffeine causes a Ca2+-induced release of Ca2+ (the CROC) from the S.R. and that the consequent rise in [Ca2+]i promotes the ultrastructural damage observed. 4. Myofibril degradation is also produced by treatment of the muscle with the divalent cation ionophore A23187; this effect is not protected by either procaine or Dantrolene sodium. 5. It is suggested that A23187 causes the release of Ca2+ from the S.R. by a mechanism that differs from both excitation and the CROC; the resultant rise in [Ca2+]i again causes myofibril degradation. 6. The ways in which a marked rise in [Ca2+]i could cause muscle damage and the possible relevance of these findings to the sequence of events in the development of myopathies of human skeletal muscle are discussed.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    Springer
    Cell & tissue research 173 (1976), S. 193-209 
    ISSN: 1432-0878
    Schlagwort(e): Muscle ; Ionophore A23187 ; Calcium ; Muscular dystrophy
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin
    Notizen: Summary The divalent cation ionophore A23187 has three major effects on the thin cutaneous pectoris muscle of frog: (1) The membrane potential is depolarized, an action that is found only when the [Ca2+] of the bathing saline is very low. (2) It causes an increase in resting tension and the development of contraction. This action is produced at both normal and low values of [Ca2+]o and is, therefore, independent of Ca2+ entry and of changes in Em. The ionophore is believed to act primarily by releasing Ca2+ from intracellular stores. (3) It causes major ultrastructural damage to the muscle filaments. It is believed that this damage is the result of the action of A23187 on the sarcoplasmic reticulum and the elevation of [Ca2+]i and we suggest that the action of this ionophore may serve as a useful model for the study of certain myopathies.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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