Fluoride (F) is highly electronegative anion with cumulative toxic effects, from prolonged ingestion that can lead to the pathogenesis known as fluorosis, a condition especially persistent in third world countries, where populations have little choice as to the main source of F-contaminated drinking. In recent times many neurological problems among children are being addressed in endemic areas. Thereby reasons for the neurotoxicity have to be explicated thoroughly. In this study premated Wistar albino rats were exposed to 50 and 150 ppm fluoride in drinking water during gestation and pups born to them were used to analyze the extent of neurotoxicity imposed in discrete brain areas. Dose dependent toxicity was evident in different brain regions and fluoride exposure has significantly enhanced the levels of malondialdehyde (P>0.05), glutathione (P>0.05) and decreased the activities of superoxide dismutase (P>0.05), catalase (P>0.05), glutathione peroxidase (P>0.05) and glutathione- S-transferase (P>0.05). Alterations were region specific and oral supplementation of dietary antioxidants viz., vitamin-C (20mg), vitamin-E (400ug), zinc (200ug) and selenium (40ug) not only inhibited oxidative stress but also enhanced the activity of antioxidant enzymes. Thereby supplementation of antioxidants to toxicated animals significantly overcame toxic burden imposed by fluoride and therefore may be a therapeutic strategy for fluorotic victims.