Abstract
In enamel fluorosis model rats treated with sodium fluoride, secretory ameloblasts of incisor tooth germs exhibited disruption of intracellular trafficking. We examined whether heterotrimeric G proteins participated in the disruption of vesicular trafficking of the secretory ameloblast exposed to fluoride, using immunoblotting and pertussis toxin (IAP)-induced adenosyl diphosphate (ADP)-ribosylation for membrane fractions of the cell. Immunoblotting of crude membranes, post supernatants of the ameloblast, with anti-G(alpha i3/alpha o) and anti-G(alpha s) antibodies showed that Gi3 or Go proteins existed in the secretory ameloblast, but Gs protein did not. Immunoblotting of the subcellular membrane fractions indicated that the Gi3 or Go proteins were located in the Golgi membrane, but were not in the rough endoplasmic reticulum (rER) membrane. Autoradiograph of IAP-induced ADP-ribosylation, however, showed the existence of IAP-sensitive G proteins both in rER and Golgi membranes. Fluoride treatment decreased the G proteins bound to both membranes. These findings indicate that different G proteins, both of which are IAP-sensitive, are present in the rER and Golgi apparatus, and suggest that these G proteins participate in the disturbance of intracellular transport of the secretory ameloblast exposed to fluoride.
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Downregulation of miR-4755-5p promotes fluoride-induced osteoblast activation via tageting Cyclin D1.
Background Endemic fluorosis remains a major public health issue in many countries. Fluoride can cause abnormalities in osteoblast proliferation and activation, leading to skeletal fluorosis. However, its detailed molecular mechanism remains unclear. Based on a previous study, the aim of this study is to explore the role of miRNA in osteoblast
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The effects of chronic high fluoride levels on forming enamel in the rat.
Sixty-gramme rats were given either 0, 75, 100 or 150 parts/10(6) fluoride in their drinking water. After five weeks, the fluoride, the phosphorus and the protein contents of the enamel were compared in control and experimental animals at three stages of enamel development. The mineral content was reduced in pigmented
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Developmental and post-eruptive defects in molar enamel of free-ranging Eastern Grey kangaroos (Macropus giganteus) exposed to high environmental levels of fluoride
Dental fluorosis has recently been diagnosed in wild marsupials inhabiting a high-fluoride area in Victoria, Australia. Information on the histopathology of fluorotic marsupial enamel has thus far not been available. This study analyzed the developmental and post-eruptive defects in fluorotic molar enamel of eastern grey kangaroos (Macropus giganteus) from the
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Fluoride affects enamel protein content via TGF-B1-mediated KLK4 inhibition
Dental fluorosis is caused by chronic high-level fluoride (F-) exposure during enamel development, and fluorosed enamel has a higher than normal protein content. Matrix metalloproteinase 20 cleaves enamel matrix proteins during the secretory stage, and KLK4 further cleaves these proteins during the maturation stage so that the proteins can be
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The effect of fluoride on the immature enamel matrix protein of the rat.
Fluoride in drinking water decreased the total quantity of enamel matrix protein formed in rat incisors and altered the relative proportions of individual amino acids of the matrix.
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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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"Mild" Dental Fluorosis: Perceptions & Psychological Impact
The vast majority of research has found that patients, parents, and the general public alike view mild fluorosis (TF score 3) as a significant blemish of the teeth, one that is likely to embarrass the affected child to a degree that cosmetic treatment would be warranted.
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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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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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