- 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.
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
Effect of fluoride on brain of albino-rabbit - An experimental study.
Background: Fluoride is present in environment in various forms and ingested by man from solid foods, drinking water and inhaled from the air. Out of these, fluoride is present in large quantities in dissolved state in many sources of drinking water producing toxicity in man. Fluoride can cross the blood-brain
Alterations of apoptosis and expressions of Bax and Bcl-2 in the cerebral cortices of rats with chronic fluorosis
The aim of the study was to investigate the influence of chronic fluorosis on apoptosis and the expression of Bax and Bcl-2 in the cerebral cortices of rats in an attempt to elucidate molecular mechanisms. Sixty Sprague Dawley (SD) rats were divided randomly into three groups of 20 each: an
Selenium Exerts Protective Effects Against Fluoride-Induced Apoptosis and Oxidative Stress and Altered the Expression of Bcl-2/Caspase Family.
Fluoride is widely distributed in nature, and at high concentrations, it targets the kidney and especially proximal tubule epithelial cells. Selenium is a typical trace element beneficial to humans, and the role of selenium in the prevention and treatment of fluoride-induced organ damage is an important research topic. The purpose
The mitochondrial pathway is involved in sodium fluoride (NaF)-induced renal apoptosis in mice.
The objective of the present study was to explore the molecular mechanism of apoptosis induced by sodium fluoride (NaF) in the mouse kidney by using the methods of flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and experimental pathology. 240 four-week-old ICR mice were randomly divided into 4
Related Studies :