Vitamin C and E in Fluoride Induced Uterine Oxidative Stress and Apoptotic Gene Expression in Wistar Rats

Management of fluoride (F) driven abnormalities is a great challenge. The present study emphasized on the abrogation of F facilitated uterine dysfunction by vitamin C and E. In the present investigation Wistar rats were fed with 200 ppm NaF at the dose of 10 mg/kg body weight orally for 28 days along with co-treatment with vitamin C and E at the doses of 50 mg/kg body weight and 15 mg/kg body weight, respectively. F treated group presented a concomitant decrease in the activity of uterine superoxide dismutase (SOD) and catalase (CAT). F ingestion developed up-regulation of tumor necrosis factor (TNF-α) and nuclear factor κB (NF-κB). The pro-apoptotic genes Bax and p53 expressions in uterine tissue were raised in response to fluoridation followed by suppression of anti-apoptotic gene Bcl-2. Vitamin C and E employed its constructive action against F intoxication by weakening TNF-α and NF-κB followed by a promotion of Bcl-2 expression along with Bax and p53 suppression. However, present investigation established the anti-oxidative, anti-inflammatory and anti-apoptotic events of Vitamin C and E.