Abstract
Five-day-old Wistar rats were given three intraperitoneal injections at 2-hourly intervals of a solution of sodium fluoride in 0.9 per cent sodium chloride. Three fluoride levels were used: a mottling dose of 3 mgF/kg body weight; and two sub-mottling doses, 0.05 mg and 0.01 mgF/kg body weight. Thirty minutes after the last injection, each rat received 5 ?Ci/g body weight of [3H]-serine. The design allowed for within-litter comparisons of treatments to be made. Rats were killed 1 hr and 20 hr after the injection of the label, and the tissues were processed for light microscope autoradiography.
After 1 hr, there was a reduced uptake with the mottling dose and an increased uptake with the smaller sub-mottling dose of fluoride. However, there was not a uniformly parallel pattern at 20 hr.
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Dental fluorosis: variability among different inbred mouse strains.
Concurrent with the decline in dental caries has been an increase in the prevalence of dental fluorosis, a side-effect of exposure to greater than optimal levels of fluoride during amelogenesis. The mechanisms that underlie the pathogenesis of dental fluorosis are not known. We hypothesize that genetic determinants influence an individual's
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Histone acetyltransferase promotes fluoride toxicity in LS8 cells.
Highlights Fluoride activates histone acetyltransferase (HAT) in enamel organ-derived LS8 cells. HAT inhibitors suppressed fluoride-mediated acetylation of p53 and cell toxicity. Modulation of HAT activity may be a potential target to mitigate fluoride toxicity. Previously we demonstrated that fluoride increased acetylated-p53 (Ac-p53) in LS8 cells that are derived from mouse enamel
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Fine mapping of dental fluorosis quantitative trait loci in mice.
Genetic factors underlie the susceptibility and the resistance to dental fluorosis (DF). The A/J (DF susceptible) and 129P3/J (DF resistant) mouse strains have previously been used to detect quantitative trait loci (QTLs) associated with DF on chromosome (Chr) 2 and Chr 11. In the present study, increased marker density genotyping
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Fluoride-induced ultrastructural changes in exocrine pancreas cells of rats: fluoride disrupts the export of zymogens from the rough endoplasmic reticulum (rER).
Influence of fluoride on exocrine pancreas cells was examined morphologically with traditional and prolonged osmium fixation techniques for electron microscopy in the enamel fluorosis model rats injected subcutaneously twice a day with 20 mg/kg body weight of sodium fluoride. Although the rough endoplasmic reticulum (rER) of exocrine pancreas cells in
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Fluorosed mouse ameloblasts have increased SATB1 retention and Gaq activity
Dental fluorosis is characterized by subsurface hypomineralization and increased porosity of enamel, associated with a delay in the removal of enamel matrix proteins. To investigate the effects of fluoride on ameloblasts, A/J mice were given 50 ppm sodium fluoride in drinking water for four weeks, resulting serum fluoride levels of
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Dental Fluorosis Is a "Hypo-mineralization" of Enamel
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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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Diagnostic Criteria for Dental Fluorosis: The TSIF ("Total Surface Index of Fluorosis")
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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Racial Disparities in Dental Fluorosis
In 2005, the Centers for Disease Control published the results of a national survey of dental fluorosis conducted between 1999 and 2002. According to the CDC, black children in the United States have significantly higher rates of dental fluorosis than either white or Hispanic children. This was not the first time that black children were found to suffer higher rates of dental fluorosis. At least five other studies -- dating as far back as the 1960s -- have found black children in the United States are disproportionately impacted by dental fluorosis.
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