Lipid peroxidation as a mechanism of injury in cardiac myocytes.
lipid peroxidation was initiated and facilitated in isolated adult heart cells by treating the cells with different concentrations of either diamide or cumene hydroperoxide. Both reagents can lower the cellular level of reduced glutathione, diamide, by oxidizing preferentially the -SH groups and cumene hydroperoxide by acting as a substrate for glutathione peroxidase and/or initiating lipid peroxidation. Examination by electron microscopy revealed that 2 x 10(-4) diamide or 0.1 mM cumene induced severe ultrastructural changes within 1 hour of treatment. The most prominent changes were contraction, severe blebbing of the plasma membrane, and the presence of mitochondrial inclusions. A severe decline in intracellular ATP accompanied these ultrastructural changes. Diene conjugation, as an index of lipid peroxidation, demonstrated that peroxidation of cellular lipids did not occur in all cell samples treated (diamide greater than cumene). Treatment of these cells with lipid peroxides produced enzymatically in liver microsome membranes gave additional confirmation that heart cells are particularly sensitive to this treatment and that lipid peroxidation could have an important role in myocardial damage.
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D001391:Azo Compounds / Q000494:pharmacology*; D001555:Benzene Derivatives / Q000494:pharmacology*; D003958:Diamide / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D050356:Lipid Metabolism; D008297:Male; D008854:Microscopy, Electron; D008856:Microscopy, Fluorescence; D008861:Microsomes / Q000187:drug effects; D008862:Microsomes, Liver / Q000378:metabolism; D008929:Mitochondria, Heart / Q000648:ultrastructure; D009206:Myocardium / Q000032:analysis / Q000166:cytology* / Q000648:ultrastructure; D051381:Rats
D001391:Azo Compounds; D001555:Benzene Derivatives; D003958:Diamide; D000255:Adenosine Triphosphate; C007164:cumene hydroperoxide