Source:http://linkedlifedata.com/resource/pubmed/id/17439417
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5-6
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| pubmed:dateCreated |
2007-4-18
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| pubmed:abstractText |
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.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Ascorbic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Catalase,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Malondialdehyde,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Fluoride,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxide Dismutase,
http://linkedlifedata.com/resource/pubmed/chemical/Vitamin E
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| pubmed:status |
MEDLINE
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| pubmed:issn |
0305-1870
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
34
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
467-74
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| pubmed:meshHeading |
pubmed-meshheading:17439417-Animals,
pubmed-meshheading:17439417-Antioxidants,
pubmed-meshheading:17439417-Apoptosis,
pubmed-meshheading:17439417-Ascorbic Acid,
pubmed-meshheading:17439417-Body Weight,
pubmed-meshheading:17439417-Catalase,
pubmed-meshheading:17439417-Disease Models, Animal,
pubmed-meshheading:17439417-Endometrium,
pubmed-meshheading:17439417-Epithelium,
pubmed-meshheading:17439417-Female,
pubmed-meshheading:17439417-Glutathione Peroxidase,
pubmed-meshheading:17439417-In Situ Nick-End Labeling,
pubmed-meshheading:17439417-Malondialdehyde,
pubmed-meshheading:17439417-Organ Size,
pubmed-meshheading:17439417-Oxidative Stress,
pubmed-meshheading:17439417-Rats,
pubmed-meshheading:17439417-Rats, Wistar,
pubmed-meshheading:17439417-Sodium Fluoride,
pubmed-meshheading:17439417-Superoxide Dismutase,
pubmed-meshheading:17439417-Uterine Diseases,
pubmed-meshheading:17439417-Uterus,
pubmed-meshheading:17439417-Vitamin E
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| pubmed:articleTitle |
Protective effects of vitamins C and E against endometrial damage and oxidative stress in fluoride intoxication.
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| pubmed:affiliation |
Department of Obstetrics and Gynecology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey. mguney@med.sdu.edu.tr
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| pubmed:publicationType |
Journal Article
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