Iron oxide nanoparticles mediated cytotoxicity via PI3K/AKT pathway: role of quercetin.

Recently Fe2O3 NPs (iron oxide nanoparticles) have been extensively used in medical imaging and in industry also. As a result, people are increasingly exposed day by day to those nanoparticles. The adverse effect of Fe2O3 NPs is not so significant at lower doses but at higher doses Fe2O3 NPs causes significant damage to cells. The present study investigates the cell signaling mechanism of Fe2O3 NPs induced oxidative stress and cytotoxicity in vitro using murine hepatocytes as the working model. In addition, the cytoprotective action of quercetin in this pathophysiology has also been investigated. Dose-dependent studies suggest that incubation of hepatocytes with 250 μg/ml Fe2O3 NPs for 4h significantly decreased the cell viability and intra-cellular antioxidant ability. This study also showed that exposure to Fe2O3 NPs caused hepatocytes death via apoptotic pathway. Incubation of hepatocytes with quercetin (50 μmol/L) prior to 1h of Fe2O3 NPs exposure protects the cells from the altering activities of antioxidant indices, cytotoxicity and apoptotic death. Results suggest that Fe2O3 NPs induced cellular damage and quercetin plays a protective role in Fe2O3 NPs induced cytotoxicity and apoptotic death.