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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.
