Abstract
Chronic fluoride exposure from drinking water may result in endemic fluorosis. To better understand the mechanisms by which some people are resistant to fluorosis, here we investigated the effect of treatment with NaF (sodium fluoride) on production of reactive oxygen species (ROS), morphological changes in mitochondria, the mRNA expression of Fas ligand (Fas‐L), and the protein expression of cleaved caspase‐3 in regular L‐929 cells and fluoride‐resistant (FR) L‐929 cells. While morphological changes indicative of apoptosis and a network of fragmented mitochondria were observed in regular L‐929 cells after NaF treatment, there were no morphological changes in FR L‐929 cells after NaF treatment. Treatment with 10 mm NaF induced a significant difference in the production of ROS, triggered the expression of cleaved caspase‐3, and upregulated the mRNA expression of Fas‐L in regular L‐929 cells. However, there was no significant production of ROS in FR L‐929 cells. Additionally, cleaved caspase‐3 and upregulated Fas‐L were not detected in FR L‐929 cells. These results suggest that FR fibroblasts are resistant to oxidative stress and apoptosis induced by fluoride.
Highlights
Rong Shu and Yiming Li contributed to this work and should be considered cocorresponding author
To better understand the mechanisms by which some people are resistant to fluorosis, here we investigated the effect of treatment with sodium fluoride (NaF) on production of reactive oxygen species (ROS), morphological changes in mitochondria, the mRNA expression of Fas ligand (Fas-L), and the protein expression of cleaved caspase-3 in regular L-929 cells and fluoride-resistant (FR) L-929 cells
Cleaved caspase-3 and upregulated Fas-L were not detected in FR L-929 cells. These results suggest that FR fibroblasts are resistant to oxidative stress and apoptosis induced by fluoride
Summary
Rong Shu and Yiming Li contributed to this work and should be considered cocorresponding author. 5% of children do not suffer from dental fluorosis in high-fluoride areas [4]. These findings imply variations in individual susceptibility to the same level of fluoride exposure within the same population. The A/J mouse strain was highly susceptible to dental fluorosis, which progressed rapidly; the 129P3/J mouse strain was more resistant, manifesting mild dental fluorosis [5,6]. All these results show that individual susceptibility to fluoride exposure varies. The molecular mechanisms of fluoride resistance responsible for such variations are poorly understood
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