- 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.
High-fluoride promoted phagocytosis-induced apoptosis in a matured ameloblast-like cell line
Endocytosis and phagocytosis are important physiologic activities occurring during ameloblast differentiation. We have previously found that excess fluoride inhibited ameloblasts endocytotic functions. Here, we hypothesized that increasing amounts of fluoride may affect ameloblast phagocytotic function during their differentiation. Using cell culture, we first induced maturation of the mouse ameloblast-like LS8
Fluoride induced endoplasmic reticulum stress and calcium overload in ameloblasts
OBJECTIVE: The aim of the study was to evaluate the involvement of endoplasmic reticulum stress and intracellular calcium overload on the development of dental fluorosis. METHODS: We cultured and exposed rat ameloblast HAT-7 cells to various concentrations of fluoride and measured apoptosis with flow cytometry and intracellular Ca2+ changes using confocal
The toxic effect of sodium fluoride on Spodoptera frugiperda 9 cells and differential protein analysis following NaF treatment of cells.
Highlights High concentrations of NaF changes Sf9 cell morphology. Cell viability decreased along with NaF concentration increased. Half-inhibitory concentration (IC50) for NaF of 5919 µM at 72 h. NaF induced cells apoptosis and dysregulation of protein expression. Accumulation of excess fluoride has a destructive effect on the environment, endangering human health,
Protective properties of sesamin against fluoride-induced oxidative stress and apoptosis in kidney of carp (Cyprinus carpio) via JNK signaling pathway.
Sesamin, a major lignan derived from sesame seeds, has been reported to have many benefits and medicinal properties. However, its protective effects against fluoride-induced injury in kidney of fish have not been clarified. Previously we found that fluoride exposure caused damage and apoptosis in the kidneys of the common carp,
Toxic effects of fluoride on reproductive ability in male rats: sperm motility, oxidative stress, cell cycle, and testicular apoptosis.
To investigate the effects of sodium fluoride (NaF) on sperm motility, oxidative stress, and apoptosis in the testes, male Wistar rats were exposed to 1.0, 2.0, and 3.0 mg NaF/kg bw/day by intragastric gavage for 90 days. Sperm motility was significantly inhibited, especially at the lower F intake level. Significant
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