LIPID-PEROXIDATION AS A MECHANISM OF INJURY IN CARDIAC MYOCYTES

  • 1 January 1982
    • journal article
    • research article
    • Vol. 47  (4) , 346-353
Abstract
Lipid peroxidation was initiated and facilitated in isolated adult [rat] heart cells by treating the cells with different concentrations of 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 EM revealed that 2 .times. 10-4 M diamide or 0.1 mM cumene induced severe ultrastructural changes within 1 h 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 configuration, as an index of lipid peroxidation, demonstrated that peroxidation of cellular lipids did occur in all cell samples treated (diamide > 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.