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

Reoxygenation of hypoxic (120 min at 37-degrees) rabbit kidney cortica l slices in vitro resulted in a rapid increase in lipid peroxidation a nd phosphatidylinositol hydrolysis. No changes in phosphatidylinositol breakdown occurred during hypoxia or upon reoxygenation in the absenc e of calcium. Incubation of renal slices with carbon tetrachloride res ulted in increased lipid peroxidation but had no effect on phosphatidy linositol breakdown. It is concluded that altered intracellular calciu m homeostasis during reoxygenation is involved in mediating increased phosphatidylinositol hydrolysis through activation of a specific phosp holipase C, but that oxidative stress per se does not have a significa nt effect on the inositol phosphate secondary messenger response in th is model system.