Biochemical Antioxidant Effects of Ellagic Acid Against Di-(n)-butyl Phthalate–Induced Oxidative Stress in Rat Brain Tissue
TL;DR
It is indicated that DBP disrupts redox homeostasis by inducing lipid peroxidation, while EA mitigates this effect through restoration of antioxidant defenses.
Abstract
Di-n-butyl phthalate (DBP), a widely used plasticizer, induces oxidative stress and neurotoxicity through the generation of reactive oxygen species. Ellagic acid (EA), a natural polyphenolic antioxidant, may counteract these effects. This study aimed to evaluate the protective role of EA against DBP-induced oxidative brain injury. Thirty-two male rats were randomly divided into four groups: Control, DBP, EA, and DBP+EA. DBP was administered orally at a dose of 500 mg/kg/day, while EA was given by gavage at 2 mg/kg/day for four weeks. Oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities were analyzed in brain tissue. DBP exposure significantly increased TBARS levels while decreasing GSH and SOD activities, indicating lipid peroxidation and antioxidant depletion. In contrast, CAT activity was elevated, suggesting a compensatory enzymatic response to excess hydrogen peroxide. EA treatment markedly attenuated oxidative damage by restoring GSH and SOD levels and normalizing CAT activity. These findings indicate that DBP disrupts redox homeostasis by inducing lipid peroxidation, while EA mitigates this effect through restoration of antioxidant defenses.