Cellular Apoptosis, Mitochondrial Swelling, Permeability and Cytochrome-C Level After (Fe3o4)-Nps Nanoparticles Exposure and Protective Role of Diferuloylmethane in Rats Liver

Abstract

During recent years the defensive role of diferuloylmethane against oxidative stress and apoptosis has been experimentally documented. Fe3O4-NPs can cause cellular death by inducing oxidative stress. Present study aimed to investigate whether diferuloylmethane could protect rats mitochondria against Fe3O4-NPs intoxication. Twenty adult male rats were randomly chosen and divided into four groups: control; treated with 10 mg/kg/d of Fe3O4-NPs; treated with diferuloylmethane at the dose 20 ml/kg/d; treated with Fe3O4-NPs (10 mg/kg/d) and diferuloylmethane (20 ml/kg/d) respectively for 28 days. The results showed that Fe3O4-NPs increased the Alanine aminotransferase (ALT), aspartate aminotransferase (AST), lipid peroxidation, mit-GSH (Glutathione), mit-CAT (Catalase), mit-GST (Glutathione S-transferase) and decreased mit-GPx (Glutathione peroxidase), with increased in mitochondrial swelling and permeability followed by the increasing level of plasmatic Cyt-c. The addition of diferuloylmethane (DFM) to these samples reduces or corrects the amount of the most of biomarkers. These findings have demonstrated that DFM can act as an antioxidant and antiapoptotic factor against damages induced by Fe3O4-NPs.