Cellular damage, induced by either A23187 (2 X 10(−5)M) or 2,4-dinitrophenol (DNP) (10(−3)M), has been studied in incubated mouse soleus muscle and has been monitored by electron microscopy and measurement of creatine kinase (CK) efflux. CK efflux induced by DNP was dependent on extracellular Ca, whereas the characteristic myofilament breakdown was not. Chlorpromazine (2 X 10(−4)M; an inhibitor of phospholipase A (PLA2] or 5 X 10(−6)M-nordihydroguaiaretic acid (NDGA) (a lipoxygenase inhibitor) almost completely inhibited CK efflux, following treatment with either A23187 or DNP, but did not affect myofilament damage. It is concluded that there are at least two separate pathways in cellular damage: (1) PLA2 activation and lipoxygenase activity culminating in sarcolemma damage and (2) a system that produces characteristic destruction of the myofilament apparatus.
JOURNAL ARTICLE|
01 February 1987
Different mechanisms mediate structural changes and intracellular enzyme efflux following damage to skeletal muscle
C.J. Duncan,
C.J. Duncan
Department of Zoology, University of Liverpool, UK.
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M.J. Jackson
M.J. Jackson
Department of Zoology, University of Liverpool, UK.
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C.J. Duncan
Department of Zoology, University of Liverpool, UK.
M.J. Jackson
Department of Zoology, University of Liverpool, UK.
Online Issn: 1477-9137
Print Issn: 0021-9533
© 1987 by Company of Biologists
1987
J Cell Sci (1987) 87 (1): 183–188.
Citation
C.J. Duncan, M.J. Jackson; Different mechanisms mediate structural changes and intracellular enzyme efflux following damage to skeletal muscle. J Cell Sci 1 February 1987; 87 (1): 183–188. doi: https://doi.org/10.1242/jcs.87.1.183
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