Oxygen radical-induced tissue injury

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Phospholipid-hydrolyzing activities were examined in rat hearts with ischemia induced by occlusion of the left main coronary artery. When homogenates of ischemic heart were incubated in vitro at 37 ﾟC, a significant amount of phosphatidylethanolamine (PE) was degraded, whereas the contents of other phospholipids did not change significantly. During the incubation, a stoichiometrical amount of lysoPE bearing mainly saturated fatty acids, whose composition resembled that of fatty acids detected at the sn-1 position in the glycerol backbone of heart PE, was formed concomitantly. No appreciable PE degradation was observed in homogenates prepared from nonischemic heart. No difference in phospholipase activities was found between ischemic and nonischemic heart homogenates when exogenous radioactive phospholipids were used as substrates. Anti-rat type II phospholipase A_2(PLA_2) antibody suppressed the degradation of PE observed in ischemic heart homogenates. These findings indicate that type II PLA_2 activity may be involved in the breakdown of endogenous PE in ischemic heart homogenates.Activation of type II PLA_2, leading to hydrolysis of endogenous PE, was also observed in other oxygen radical-induced tissue injury, such as CCl_4-treated rat liver. Certain lipid-derived compound(s), which activated type II PLA_2, were detected in homogenate of CCl_4-treated liver. In the presence of lipids derived from CCl_4-treated liver, type II PLA_2 was significantly activated at lower (10^<-6> to 10^<-5> M) Ca^<2+> concentrations. Production of peroxidized lipids might explain the progressed breakdown of endogenous PE by type II PLA_2 in oxygen-injured tissues.