Abstract
1. Fluoride (F) is an essential trace element that has protective effects against bone mineral loss. However, it becomes toxic at higher doses and induces some adverse effects on a number of physiological functions, including reproduction. The aims of this study were to examine F-induced oxidative stress that promotes production of reactive oxygen species (ROS) and to investigate the role of vitamins C and E against possible F-induced endometrial impairment in rats. 2. Rats were divided into three groups: control, F and F plus vitamins. The F group was given 100 mg/L orally for 60 days. Combined vitamins were also administered orally. Fluoride administration to control rats significantly increased endometrial malondialdehyde (MDA) but decreased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities. Endometrial glandular and stromal apoptosis were investigated by DNA nick end-labelling (TUNEL) method on each sample and the mean endometrial apoptotic index (AI) was calculated. 3. Vitamin administration with F treatment caused endometrial MDA to decrease, but SOD, GSH-Px and CAT activities to increase, all to significant levels. Vitamins showed a histopathological protection against F-induced endometrial damage. There was a significant difference in the AI between the groups. Lymphocyte and eosinophil infiltration in stroma in F-treated rats were more than those in the control and F + Vit groups. 4. It can be concluded that oxidative endometrial damage plays an important role in F-induced endometrial toxicity, and the modulation of oxidative stress with vitamins reduces F-induced endometrial damage both at the biochemical and histological levels.