Further evidence of centrophenoxine mediated protection in aluminium exposed rats by biochemical and light microscopy analysis.

The environmental agent aluminium has been intensively investigated in the initiation and progression of various neurological disorders and the role of oxidative stress in these disorders is a widely discussed phenomenon. In this light, the present study is focused on the role of aluminium in mediating oxidative stress, which may help in better understanding its role in neuronal degeneration. Further, we have exploited a known anti-aging drug centrophenoxine to explore its potential in the conditions of metal induced oxidative damage. Aluminium was administered orally at a dose level of 100 mg/kg b.wt./day for a period of 6 weeks followed by a post treatment of centrophenoxine at a dose level of 100 mg/kg b.wt./day for another 6 weeks. Following aluminium exposure, a significant increase in lipid peroxidation levels (estimated by MDA) were observed which was accompanied by a decrease in reduced glutathione content in both cerebrum and cerebellum of rat brain. Post treatment of centrophenoxine significantly reduced the lipid peroxidation levels and also increased the reduced glutathione content in both the regions. Histologically observed marked deteriorations in the organization of various cellular layers in both cerebrum and cerebellum were observed after aluminium administration. Centrophenoxine treated animals showed an appreciable improvement in the histoarchitecture of the cellular layers. Our results indicate that centrophenoxine has an antioxidant potential and should be examined further in aluminium toxic conditions.