Mitochondrial enzyme retention by irreversibly damaged rectangular isolated adult rat heart myocytes.
A one hour hypoxic incubation causes the release of a small but significant amount of cytosolic lactic dehydrogenase from glucose-deprived isolated adult rat heart myocytes. However, enzymes associated with the mitochondria are not liberated, and there is no increase in the number of hypercontracted cells. These observations led Piper et al. (Life Sciences 35, 127-134 [1984]) to conclude that reversibly injured myocytes can release cytosolic proteins. This conclusion was based on the supposition that irreversibly hypoxic injury must cause mitochondrial enzyme efflux and hypercontracture. The present study establishes that this supposition is invalid.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D003402:Creatine Kinase / Q000378:metabolism; D003600:Cytosol / Q000201:enzymology; D004072:Digitonin / Q000494:pharmacology; D005969:Glutamate Dehydrogenase / Q000378:metabolism; D000860:Hypoxia / Q000201:enzymology; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008291:Malate Dehydrogenase / Q000378:metabolism; D008854:Microscopy, Electron; D008929:Mitochondria, Heart / Q000201:enzymology*; D009206:Myocardium / Q000166:cytology / Q000473:pathology*; D010101:Oxygen Consumption; D051381:Rats; D013997:Time Factors
D007527:Isoenzymes; D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; D008291:Malate Dehydrogenase; D005969:Glutamate Dehydrogenase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase; D004072:Digitonin