Effects of hyperoxia and acrylonitrile on the phospholipase C isozyme protein levels in rat heart and brain

We previously showed that hyperoxia exerts oxidative stress on the rat cerebral cortex, and the protein levels of phospholipase C (PLC) -β1 and -δ1, but not PLC-γ1, were changed. Acrylonitrile (ACN) appears to induce astrocytomas through induction of oxidative stress on the rat brain selectively. This study compared hyperoxia or ACN treatments of rats with respect to lipid peroxidation and PLC levels in the heart and cerebral cortex. Treatment of rats with ACN promoted lipid peroxidation in the heart and cerebral cortex, the percent increase above control being greater in the cortex than heart. Hyperoxia did not cause significant increases in lipid peroxidation in the cerebral cortex or heart. In the ACN-treated cerebral cortex, significant increases in the PLC-β1 and -δ1 in the cytosol, and PLC-γ1 in the cytosolic and particulate fractions, and lysate were observed. In the rat heart, in which PLC-β1 could not be detected, PLC-γ1 and -δ1 were increased and decreased in the cytosolic and particulate fractions, respectively, by hyperoxia. In addition, the expression level of PLC-γ1 was decreased in the lysate by the treatment. In the heart treated with ACN, there was no change in the level of PLC-γ1, while PLC-δ1 was elevated in all fractions. These findings suggested that the expression levels of PLC isozymes are altered by hyperoxia and ACN, but there are apparent differences in these altered levels between the different levels of oxidative stress, and between the organs.