title: Protective effects of vitamins C and E against endometrial damage and oxidative stress in fluoride intoxication.
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.
authors: Department of Obstetrics and Gynecology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey. mguney@med.sdu.edu.tr
authors: Mehmet
authors: M
authors: Guney
authors: Baha
authors: B
authors: Oral
authors: Hilmi
authors: H
authors: Demirin
authors: Nermin
authors: N
authors: Karahan
authors: Tamer
authors: T
authors: Mungan
authors: Namik
authors: N
authors: Delibas
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D001205:Ascorbic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D001835:Body Weight / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D004717:Endometrium / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D008315:Malondialdehyde / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D012969:Sodium Fluoride / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000633:toxicity*; D013482:Superoxide Dismutase / Q000378:metabolism; D014591:Uterine Diseases / Q000139:chemically induced / Q000517:prevention & control*; D014599:Uterus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D014810:Vitamin E / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D000975:Antioxidants; D014810:Vitamin E; D008315:Malondialdehyde; D012969:Sodium Fluoride; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001205:Ascorbic Acid