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

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.