- TiF4 and NaF varnishes have similar apoptosis effects on NIH/3T3 and HGF.
- HGF is more susceptible to the effect of the fluoride varnishes than NIH/3T3.
- TiF4 and NaF varnishes induce a low activation of apoptosis mechanisms.
- The low cytotoxic effect TiF4 varnish supports testing it in clinical trials.
Objectives: This study evaluated the level and mechanism of apoptosis in human gingival fibroblasts (HGF) and murine fibroblasts (NIH/3T3) treated with a titanium tetrafluoride (TiF4) varnish compared those treated with a sodium fluoride (NaF) varnish.
Methods: Cells were treated with a TiF4, NaF (both 2.45%F) or placebo varnish for 6?h and were then examined using the TUNEL method. The activities of caspase-3, -8 and -9 were assessed. cDNA for Bax, Bad, Bcl-2 and Fas-L was amplified by quantitative PCR. Bax, Bcl-2 and Fas-L were further detected by western blot analysis.
Results: Both fluorides similarly increased the percentage of apoptosis, while they failed to activate caspases. The Bax/Bcl-2 gene expression ratio was not altered by either fluoride treatment regardless of the type of cell. NaF varnish increased the amplification of the Fas-L gene in NIH/3T3 and HGF cells, while treatment with the TiF4 varnish resulted in a lower Bad/Bcl-2 expression ratio compared to that of the control for NIH/3T3 cells, but not for HGF cells. No effect of the fluorides was detected in the protein analysis.
Conclusions: NaF and TiF4, at the studied conditions, similarly induce a low level of apoptosis, with consequent modest activation of the Bcl-2 and Fas-l-dependent signalling pathways. Generally, HGF cells are more susceptible to the fluoride effect than NIH/3T3 cells.
Sodium fluoride promotes apoptosis by generation of reactive oxygen species in human lymphocytes
Fluoride generated the attention of toxicologists due to its deleterious effects at high concentrations in human populations suffering from fluorosis and in in vivo experimental models. Interest in its undesirable effects has resurfaced due to the awareness that this element interacts with cellular systems even at low doses. This study
Simultaneous administration of fluoride and selenite regulates proliferation and apoptosis in murine osteoblast-like MC3T3-E1 cells by altering osteoprotegerin.
The receptor activator nuclear factor kappa-B ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG), are important for maintaining the balance between bone formation and resorption. However, the regulation of microelements on these factors remains unclear. In this study, we used murine osteoblast-like MC3T3-E1 cells to examine the impact of sodium
Sodium fluoride induces apoptosis through the downregulation of hypoxia-inducible factor-1a in primary cultured rat chondrocytes
It has been reported that sodium fluoride (NaF) suppresses the proliferation and induces apoptosis of chondrocytes. However, the cellular and molecular mechanisms of the effect have not been elucidated. Therefore, the aim of this study was to evaluate the mechanisms of the effects of NaF on primary cultured rat chondrocytes
Fluoride induces apoptosis in H9c2 cardiomyocytes via the mitochondrial pathway.
Highlights We studied the toxic effects of different concentrations of NaF in H9c2 cells. NaF inhibited H9c2 cell proliferation and induced early apoptosis. Mitochondrial membrane potential decreased with increase in NaF. Caspase-3, caspase-9, and cytochrome c mRNA levels increased with increase in NaF. Fluoride induces apoptosis via activation of the
Micromolar fluoride alters ameloblast lineage cells in vitro.
Fluorosed enamel is caused by exposure to fluoride during tooth formation. The objective of this study was to determine whether epithelial ameloblast-lineage cells, derived from the human enamel organ, are directly affected by micromolar concentrations of fluoride. Cells were cultured in the presence of fluoride, and proliferation was measured by
Related Studies :