Protective effects of vitamins C and E against endometrial damage and oxidative stress in fluoride intoxication

Clin Exp Pharmacol Physiol. May-Jun 2007;34(5-6):467-74. doi: 10.1111/j.1440-1681.2007.04596.x.


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.

MeSH terms

  • Animals
  • Antioxidants / pharmacology
  • Antioxidants / therapeutic use
  • Apoptosis / drug effects
  • Ascorbic Acid / pharmacology*
  • Ascorbic Acid / therapeutic use
  • Body Weight / drug effects
  • Catalase / metabolism
  • Disease Models, Animal
  • Endometrium / drug effects*
  • Endometrium / metabolism
  • Endometrium / pathology
  • Epithelium / drug effects
  • Epithelium / metabolism
  • Epithelium / pathology
  • Female
  • Glutathione Peroxidase / metabolism
  • In Situ Nick-End Labeling
  • Malondialdehyde / metabolism
  • Organ Size / drug effects
  • Oxidative Stress / drug effects*
  • Rats
  • Rats, Wistar
  • Sodium Fluoride / administration & dosage
  • Sodium Fluoride / antagonists & inhibitors
  • Sodium Fluoride / toxicity*
  • Superoxide Dismutase / metabolism
  • Uterine Diseases / chemically induced
  • Uterine Diseases / prevention & control*
  • Uterus / drug effects
  • Uterus / metabolism
  • Uterus / pathology
  • Vitamin E / pharmacology*
  • Vitamin E / therapeutic use


  • Antioxidants
  • Vitamin E
  • Malondialdehyde
  • Sodium Fluoride
  • Catalase
  • Glutathione Peroxidase
  • Superoxide Dismutase
  • Ascorbic Acid