Neurotoxic profiles of vanadium when administered at the onset of myelination in rats: the protective role of vitamin E
Vanadium has been reported to cause oxidative stress and subsequent neurotoxicity. In this study, we exposed neonatal rats at the onset and peak of myelination to vanadium and examined the protective effect of Vitamin E to the resulting neurotoxic effects. Neonatal rats were given sodium metavanadate (SMV) intraperitoneally (i.p) at 3mg/kg body weight (b.w) daily from postnatal day 12 to 21; a second group exposed to the same dose of SMV also had the dams receiving 500 mg/kg b.w of Vitamin E (vit E) orally every 72 hrs. A third group received vit E alone while control rats pups received sterile water administered i.p. The animals were subjected to behavioural tests prior to sacrifice on day 22 after which the brains were weighed and then subjected to histological examination. Pups exposed to vanadium showed reduced upper body strength which was protected by administration of vit E. Routine histology with Haematoxylin and Eosin revealed increased necrotic neurons of the medulla in vanadium exposed rats. Cresyl Violet stain showed depletion of the external granular layer of the cerebellum which was confirmed as neural stem cells by Nestin immunohistochemistry. Further “immune” assays revealed astrocytic activation (GFAP stain), demyelination (CNPase) and activated microglia (Iba1) due to vanadium which were ameliorated by the administration of vit E to the dams. The pups whose dams were administered with vit E alone showed signs of cellular degeneration which might be due to peroxidative effects of á-tocopherol in the absence of an oxidative stress condition. In conclusion, our study shows that vit E administration via lactation can ameliorate neuropathological changes in rats exposed to vanadium at the onset and peak of myelination process.
Keywords: Antioxidant, Neurotoxicity, External Granular layer, Cerebellum, Immunohistochemistry