REOXYGENATION FOLLOWING HYPOXIA STIMULATES LIPID-PEROXIDATION AND PHOSPHATIDYLINOSITOL BREAKDOWN IN KIDNEY CORTICAL SLICES

Reoxygenation of hypoxic (120 min at 37-degrees) rabbit kidney cortical slices in vitro resulted in a rapid increase in lipid peroxidation and phosphatidylinositol hydrolysis. No changes in phosphatidylinositol breakdown occurred during hypoxia or upon reoxygenation in the absence of calcium. Incubation of renal slices with carbon tetrachloride resulted in increased lipid peroxidation but had no effect on phosphatidylinositol breakdown. It is concluded that altered intracellular calcium homeostasis during reoxygenation is involved in mediating increased phosphatidylinositol hydrolysis through activation of a specific phospholipase C, but that oxidative stress per se does not have a significant effect on the inositol phosphate secondary messenger response in this model system.