- Fluoride is an important environmental pollutant with serious health implications.
- Fluoride exposure induce apoptotic death in IEC-6 cells via redox imbalance.
- CHE restored fluoride-induced glutathione depletion and lipid peroxidation.
- CHE treatment prevented the fluoride-induced caspase activation and apoptosis.
- Coconut haustorium may be useful against fluoride-induced health issues.
Fluoride ions are an important environmental contaminant and pollutant found in a wide variety of environmental conditions. The fluoride in drinking water is evident to induce toxic effects including neurodegeneration, skeletal and dental fluorosis as well as organ damage. Nutraceuticals and functional foods are emerging as possible preventive agents against fluoride toxicity. Hence, the possible use of an emerging functional food-the coconut haustorium is being evaluated against sodium fluoride-induced toxicity in intestinal cells (IEC-6). The cells exposed to fluoride showed significant cell death mediated through the increased lipid peroxidation and glutathione depletion. The glutathione biosynthetic enzymes were inhibited by the exposure to fluoride and the apoptotic genes (caspases 3/7 and apaf-1) were upregulated. The CHE pre-treatment improved the activity of enzymes involved in the de novo biosynthesis of glutathione and subsequently improved the intracellular GSH pool. The improved antioxidant defense was also evident from the reduced expression of apoptotic genes (p < 0.05). Overall, the study concludes that fluoride ions induce oxidative stress-mediated apoptosis in intestinal epithelial cells, via inhibiting glutathione biosynthesis. Methanol extract of coconut haustorium increased glutathione biosynthesis and subsequently prevented fluoride toxicity in IEC-6 cells by virtue of its antioxidant potentials.
*Original abstract online at https://www.sciencedirect.com/science/article/abs/pii/S0013935121010112
Significance of Inflammation and Apoptosis in Hepatocellular Death in Rat, Co-treated with Arsenic and Fluoride.
Health effects elicited by combined environmental exposures to xenobiotics, in many instances, still remain unresolved. One of these examples is the combined toxicity of arsenic and fluoride. The present study was undertaken to delineate the role of inflammation and apoptosis in hepatocellular death caused by co-exposure to arsenic and fluoride
TiF4 and NaF varnishes induce low levels of apoptosis in murine and human fibroblasts through mitochondrial Bcl-2 family and death receptor signalling.
Highlights 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
Sodium fluoride modulates caprine osteoblast proliferation and differentiation
The cellular and molecular pathways of fluoride toxicity in osteoblasts are not very well understood. Therefore, the objective of the present study was to evaluate the effects of sodium fluoride (NaF) on caprine osteoblasts cultured in vitro. Caprine osteoblasts at 2.0 x 10(-4) cells/ml were incubated in vitro with NaF
Fluoride Induces Apoptosis in Mammalian Cells: In Vitro and In Vivo Studies.
Apoptosis is genetically programmed cell death, an irreversible process of cell senescence with characteristic features different from other cellular mechanisms of death such as necrosis. In the last years, apoptosis has been extensively studied in the scientific literature, because it has been established that apoptosis plays a crucial role following
Sodium fluoride induces apoptosis in the kidney of rats through caspase-mediated pathways and DNA damage
Long-term excessive sodium fluoride (NaF) intake can cause many bone diseases and nonskeletal fluorosis. The kidneys are the primary organs involved in the excretion and retention of NaF. The objective of the present study was to determine the effects of NaF treatment on renal cell apoptosis, DNA damage, and the
Related Studies :