- 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.
Effects and Molecular Mechanism of L-Type Calcium Channel on Fluoride-Induced Kidney Injury.
This study aimed to investigate the role and molecular mechanism of L-type calcium channel (LTCC) on fluoride exposure-induced kidney injury. Subchronic and chronic fluoride exposures were included in the experiment. Each part contained 140 ICR male mice. They were randomly divided into 7 groups: control group, high-fluoride group (NaF 30
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
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
Sodium fluoride activates the extrinsic apoptosis via regulating NOX4/ROS-mediated p53/DR5 signaling pathway in lung cells both in vitro and in vivo.
An extensive body of research has demonstrated that pulmonary toxicity induced by fluoride is related to cell apoptosis. Although induction of death receptor-initiated extrinsic apoptosis by sodium fluoride (NaF) has been reported, its mechanism of action is still not clearly defined. Herein, we found that NaF treatment induced activation of
Exposure to Fluoride induces apoptosis in liver of ducks by regulating Cyt-C/Caspase 3/9 signaling pathway.
Highlights Long-term exposure NaF induced hepatotoxicity in ducks. NaF exposure caused liver granule and vacuolar degeneration observed by histological analysis. The mechanism of NaF exposure on hepatotoxicity involving activating autophagy and apoptosis. Cyt-C/Caspase 3/9 signaling pathway activation target cell death. Abstract Fluorine being a well-known and essential element for normal physiological
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