Abstract
PURPOSE: To study the effect of fluoride on autophagy in rat ameloblasts both in vitro and in vivo.
METHODS: Logarithmic-phase HAT-7 cells were cultured in different concentrations of fluoride for 48h. Transmission electron microscopy (TEM) was used to detect autophagosomes. Western blot and RT-qPCR were carried out to examine the expression of LC3 and Beclin 1. Forty Wistar rats were divided into 4 groups randomly. The expression of LC3 and Beclin 1 in rats was investigated by immunohistochemical staining in vivo. The data were analysed using SPSS13.0 software package.
RESULTS: The amount of autophagosomes in the experimental group was significantly more than that in the control group (P<0.05). The expression of LC3 and Beclin 1 were up-regulated in dose dependent manner after treatment with fluoride. Regression analysis showed that fluoride dependently induced the expression of LC3 and Beclin 1 (P<0.05).Immunohistochemical analysis revealed that the expression of LC3 and Beclin 1 in rat ameloblasts in the experimental groups was positive compared to control group.
CONCLUSIONS: Excessive fluoride induced autophagy in ameloblasts both in vitro and in vivo.
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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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Enamel crystals of mice susceptible or resistant to dental fluorosis: an AFM study
Objective: This study aimed to assess the overall apatite crystals profile in the enamel matrix of mice susceptible (A/J strain) or resistant (129P3/J strain) to dental fluorosis through analyses by atomic force microscopy (AFM). Material and Methods: Samples from the enamel matrix in the early stages of secretion and maturation were obtained
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Fluoride exposure alters Ca2+ signaling and mitochondrial function in enamel cells.
Fluoride ions are highly reactive, and their incorporation in forming dental enamel at low concentrations promotes mineralization. In contrast, excessive fluoride intake causes dental fluorosis, visually recognizable enamel defects that can increase the risk of caries. To investigate the molecular bases of dental fluorosis, we analyzed the effects of fluoride
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Dental fluorosis and a polymorphism in the COL1A2 gene in Mexican children.
Highlights Dental fluorosis is a public health problem in the communities evaluated. The rs 412777 polymorphism in the COL1A2 gene was found in Mexican children. An association between the COL1A2 gene polymorphism and dental fluorosis was found. The genetic variant evaluated represents a risk factor to develop dental fluorosis. OBJECTIVE:
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Sirtuin1 and autophagy protect cells from fluoride-induced cell stress
Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylase functioning in the regulation of metabolism, cell survival and organismal lifespan. Active SIRT1 regulates autophagy during cell stress, including calorie restriction, endoplasmic reticulum (ER) stress and oxidative stress. Previously, we reported that fluoride induces ER-stress in ameloblasts responsible for enamel formation,
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Dental Fluorosis Is a "Hypo-mineralization" of Enamel
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Severe Dental Fluorosis: Perception and Psychological Impact
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