- Fluoride causes histopathological changes in C2C12 cells.
- Fluoride exposure damages ultrastructure in C2C12 cells.
- Fluoride exposure induces apoptosis in C2C12 cells.
- PI3K/AKT signaling pathway is involved in fluoride-induced apoptosis in C2C12 cells.
To investigate the mechanisms of fluoride-induced apoptosis, a fluoride-induced C2C12 skeletal muscle cell (C2C12 cell) model was established in this study, and the viability of the C2C12 cells was measured using an MTT assay. Cell morphological changes were observed via haematoxylin and eosin staining and transmission electron microscopy. Apoptosis was monitored through Hoechst staining. The mRNA and protein expression of PI3K, PDK1, AKT1, BAD, Bcl-2, Bax and caspase-9 were detected through real-time PCR and western blotting, respectively. The results showed that the survival rates of C2C12 cells decreased gradually with an increasing fluoride doses. The C2C12 cell structure was seriously damaged by fluoride, presenting with pyknosis, mitochondrial ridge disruption and swollen endoplasmic reticulum. Furthermore, the expression of mRNA in PI3K, BAD, Bcl-2, Bax and caspase-9 were significantly increased in the fluoride group (P <0.01), while the expression of PDK1 was markedly decreased (P <0.01). The expression of protein in BAD, Bcl-2 and Bax were significantly increased in the fluoride group (P <0.01), while the expression of PDK1 and P-AKT1 was markedly decreased (P <0.01). In conclusion, fluoride-induced apoptosis in C2C12 cells is related to the PI3K/AKT signaling pathway.
Sodium fluoride induces apoptosis in mouse embryonic stem cells through ROS-dependent and caspase- and JNK-mediated pathways
Sodium fluoride (NaF) is used as a source of fluoride ions in diverse applications. Fluoride salt is an effective prophylactic for dental caries and is an essential element required for bone health. However, fluoride is known to cause cytotoxicity in a concentration-dependent manner. Further, no information is available on the
Effects of selenium and zinc on renal oxidative stress and apoptosis induced by fluoride in rats.
OBJECTIVE: To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride. METHODS: Wistar rats were given distilled water containing sodium fluoride (50 mg/L NaF) and were gavaged with different doses of selenium-zinc preparation for six months. Four groups
SIRT1 suppresses p53-dependent apoptosis by modulation of p21 in osteoblast-like MC3T3-E1 cells exposed to fluoride.
Highlights High levels of fluoride induced oxidative stress and apoptosis in MC3T3-E1 cells. Fluoride induced cell cycle arrest in the S-phase. SIRT1 attenuated fluoride-induced oxidative stress, cell cycle arrest and apoptosis. SIRT1/p53/p21 pathway is involved in the regulation of cell cycle arrest and apoptosis. Fluoride is very crucial for development of
Sodium fluoride adversely affects ovarian development and reproduction in Drosophila melanogaster.
The study demonstrates the effects of chronic sub-lethal exposure of sodium fluoride (NaF) on reproductive structure and function of female Drosophila melanogaster. As a part of treatment, flies were maintained in food supplemented with sub-lethal concentrations of NaF (10-100 ?g/mL). Fecundity, ovarian morphology, presence and profusion of viable cells from ovary
Fluorosis caused cellular apoptosis and oxidative stress of rat kidneys
As the strongest electronegative element, fluorine can stimulate the production of superoxide radicals in cells. In view of the important roles of kidneys in bone metabolism, the authors analyzed the quantitative pathomorphological characteristics of renal damage and the potential cellular apoptosis and oxidative stress mechanisms in rats treated with excessive
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