Effects of starvation on vacuolar apparatus of cardiac muscle tissue determined by electron microscopy, marker-enzyme assays and electrolyte studies.
The effects of a six day starvation regimen on rats' hearts were studied by electron microscopy in combination with marker-enzyme assays of density-sedimentation (rho-S) zonal centrifugation fractions, and with Na+, K+ and Ca++ determinations of sera and heart homogenates. The evidence suggested that massive intracellular cardiac destruction occurred by two pathways. One pathway was seen by electron micrography in which proliferation of lysosomal populations was demonstrated. The finding was confirmed biochemically by increased activities of lysosomal acid hydrolases, particularly cathepsin D. The second pathway was deduced from biochemical and electrolytic data. It was believed to have been initiated by cellular K+ retention, which provided the acid milieu required for intracellular Ca++ retention. It is postulated that the resulting increase in Ca++ activated the loosely-bound membrane neutral (pH 7.4), and alkaline (pH 8.5) proteases, causing subcellular autolysis, particularly involving mitochondria, myofibrils and sarcoplasmic reticulum.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D006867:Hydrolases / Q000378:metabolism; D008247:Lysosomes / Q000201:enzymology / Q000648:ultrastructure; D008297:Male; D008929:Mitochondria, Heart / Q000648:ultrastructure; D009206:Myocardium / Q000201:enzymology / Q000648:ultrastructure*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013217:Starvation / Q000378:metabolism / Q000473:pathology*; D014617:Vacuoles / Q000201:enzymology
D012964:Sodium; D006867:Hydrolases; D011188:Potassium; D002118:Calcium