Abstract
The status of lipid peroxidation (LPO) and antioxidants was studied in red cell blood lysates of male subjects, aged 41-50, living in an endemic fluorosis area, Vellore district, Tamil Nadu, India. The men were divided into four groups: 1) normal healthy individuals (n=10); 2) individuals with mild dental fluorosis (n=13); 3) individual with moderate dental fluorosis (n=8); 4) individuals with severe dental fluorosis (n=7). In the groups with dental fluorosis, the concentration of thiobarbituric acid reactive substances (TBARS) was higher in the red blood cell lysates along with a concomitant decrease in the levels of both enzymatic and nonenzymatic antioxidants. Statistical analysis of all the group data revealed that increased lipid peroxidation and altered antioxidant status induced by fluoride were strongly associated with the prevalence of dental fluorosis.
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Uncoupling protein-2 is an antioxidant that is up-regulated in the enamel organ of fluoride-treated rats
Dental fluorosis is characterized by subsurface hypomineralization and retention of enamel matrix proteins. Fluoride (F-) exposure generates reactive oxygen species (ROS) that can cause endoplasmic reticulum (ER)-stress. We therefore screened oxidative stress arrays to identify genes regulated by F- exposure. Vitamin E is an antioxidant so we asked if a
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Cytoprotective effects of curcumin on sodium fluoride-induced intoxication in rat erythrocytes
Curcumin is well known for its potent antioxidant activity. The result of numerous studies showed that antioxidants can protect against fluoride-induced toxicity. In the present study, protective effects of curcumin against sodium fluoride-induced toxicity in rat erythrocytes were evaluated. Curcumin (10 and 20 mg/kg) and vitamin C (10 mg/kg) were
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Effect of sodium fluoride ingestion on malondialdehyde concentration and the activity of antioxidant enzymes in rat erythrocytes
Fluoride intoxication has been shown to produce diverse deleterious metabolic alterations within the cell. To determine the effects of sodium fluoride (NaF) treatment on malondialdehyde (MDA) levels and on the activity of antioxidant enzymes in rat erythrocytes, Male Wistar rats were treated with 50 ppm of NaF or were untreated
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In vitro effect of sodium fluoride on antioxidative enzymes and apoptosis during murine odontogenesis.
Excessive fluoride ingestion has been identified as a risk factor for fluorosis and oxidative stress. The oxidative stress results from the loss of equilibrium between oxidative and antioxidative mechanisms that can produce kinase activation, mitochondrial disturbance and DNA fragmentation, resulting in apoptosis. Actually many people are exposed to no-adverted fluoride
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Oxidative stress in children with endemic skeletal fluorosis
In the village of Kheru Nayak Thanda in the Gulbarga district of Karnataka, India, 18 children aged 3 to 10 years with endemic skeletal fluorosis were shown to have oxidative stress as evidenced by elevated levels of malondialdehyde in their red blood cells, indicating increased lipid peroxidation. Significant alterations of
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Diagnostic Criteria for Dental Fluorosis: The Thylstrup-Fejerskov (TF) Index
The traditional criteria (the "Dean Index") for diagnosing dental fluorosis was developed in the first half of the 20th century by H. Trendley Dean. While the Dean Index is still widely used in surveys of fluorosis -- including the CDC's national surveys of fluorosis in the United States -- dental
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Community Fluorosis Index (CFI)
The current Community Fluorosis Index for U.S. adolescents as a whole (from both fluoridated and non-fluoridated areas) is roughly 5 times higher than the CFI health authorities predicted for fluoridated areas when fluoridation first began. It is also higher than the CFI that the NIDR found in fluoridated areas back in the 1980s. It is readily apparent, therefore, that children are ingesting far more fluoride than was the case in the 1950s, and even as recently as the 1980s.
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Mechanisms by Which Fluoride Causes Dental Fluorosis Remain Unknown
When it comes to how fluoride impacts human health, no tissue in the body has been studied more than the teeth. Yet, despite over 50 years of research, the mechanism by which fluoride causes dental fluorosis (a hypo-mineralization of the enamel that results in significant staining of the teeth) is not
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Dental Fluorosis Is a "Hypo-mineralization" of Enamel
Teeth with fluorosis have an increase in porosity in the subsurface enamel ("hypomineralization"). The increased porosity of enamel found in fluorosis is a result of a fluoride-induced impairment in the clearance of proteins (amelogenins) from the developing teeth. Despite over 50 years of research, the exact mechanism by which fluoride impairs amelogin
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Dental Fluorosis Impacts Dentin in Addition to Enamel
Dental fluorosis is a mineralization defect of tooth enamel marked by increased subsurface porosity. The enamel, however, is not the only component of teeth that is effected. As several studies have demonstrated, dental fluorosis can also impair the mineralization of dentin as well. As noted in one review: "The fact that
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