Abstract

Premated 3-month-old albino rats received 200-ppm fluoride ion (F) in their drinking water; the pups born to them were separately administered, in groups of six, daily doses of clinoptilolite, zinc, selenium, vitamin C, vitamin D, and propolis. On post-partum day 45, the pups were sacrificed, brain regions separated, and oxidative stress markers were analyzed. Prenatal (maternal) and postnatal F exposure in the developing rats caused a significant increase in the activity of lipid peroxidation and a decrease in catalase, superoxide dismutase, and glutathione peroxidase activity, thus indicating vulnerability of the developing brain to oxidative stress. Alterations were region specific, and oral supplementation of the listed antioxidants not only inhibited oxidative stress but also enhanced the activity of antioxidant enzymes. Administration of antioxidants during F exposure significantly overcame neuronal F toxicity (mostly with p<0.05 or <0.01) and therefore may be a therapeutic strategy for fluorotic victims.

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