ISSN:
1432-0878
Keywords:
Lysosomes
;
Muscle damage
;
Calcium
;
Lysosomotropic agents
;
Phospholipase A2
;
Frog (Rana temporaria)
;
Guinea pig
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
Notes:
Summary Experiments with lysosomotropic agents suggest that the sarcotubular system subserves some of the functions of the lysosomal apparatus in frog skeletal muscle. Dinitrophenol or A23187 trigger lysosome labilization and myofilament damage in mammalian cardiac muscle. Lysolecithin labilizes isolated liver lysosomes, but has no action following phospholipase A2 activation in vivo. Zinc ions or a pHi of 7.5 do not protect against myofilament damage. In fractions from mammalian cardiac muscle, calcium and calmodulin do not cause lysosomal labilization whereas cGMP does but only at high concentration (10-4 M). It is concluded that lysosomal hydrolases play no significant part in rapid muscle damage. It is suggested that rises in [Ca]i activate two separate pathways causing (i) myofilament damage; (ii) sarcolemmal (and possibly lysosomal) membrane damage via phospholipase A2 and lipoxygenase activity. Dinitrophenol triggers both pathways independently and thus may cause lysosome labilization. The possibility that the sarcoplasmic reticulum is the site generating myofilament damage is discussed.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00222302
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