Aluminium-Induced Imbalance in Oxidant and Antioxidant Determinants in Brain Regions of Female Rats: Protection by Centrophenoxine

Abstract

The present study was carried out to investigate the potential of centrophenoxine in modulating aluminium-induced neurotoxicity. Female Sprague Dawley rats were administered aluminium chloride orally (40 mg/kg b.w./day) for a period of 8 weeks. At the end of respective treatment, various markers of oxidative stress were determined in four different regions of brain: cerebrum cerebellum, medulla oblongata, and hypothalamus. Lipid peroxidation assay was also carried out using standard techniques. Simultaneously, the centrophenoxine group (100 mg/kg b.w./day) for 6 weeks was also run long to understand the role in ameliorating oxidative damage.A significant decrease in the activities of superoxide dismutase and catalase was noticed in all the four regions, the most significant being in the hypothalamus (0.603 ± .06) and cerebrum (0.038 ± .01). Due to aluminium toxicity, peroxidation of lipids was also found to be elevated in cerebrum (0.424 ± .03), cerebellum (0.341 ± .03), hypothalamus (1.018 ± .007), and medulla oblongata (0.304 ± .05). However, posttreatment with centrophenoxine significantly elevated the superoxide and catalase activities in different regions. In addition, lipid peroxidation status of membranes was significantly reduced after centrophenoxine posttreatment to aluminium-exposed animals.Centrophenoxine has proved to be beneficial in combating the damage caused by aluminium toxicity. However, further research is needed to have a better understanding of the molecular basis of aluminium-induced oxidative damage. In addition, the different aspects of centrophenoxine need to be unmasked.