- 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.
Selenomethionine alleviated fluoride-induced toxicity in zebrafish (Danio rerio) embryos by restoring oxidative balance and rebuilding inflammation homeostasis.
Highlights F induced developmental damage, oxidative stress and inflammation in embryos. Low levels of Se-Met-alone has certain adverse effects on zebrafish embryos. Se-Met-alleviated f toxicity by reducing oxidative damage and inflammation. MAPKs and NF-kB pathways may be alleviating mechanism of Se-Met-to f toxicity. Fish are target organisms that are extremely susceptible
Protective role of tert-butylhydroquinone against sodium fluoride-induced oxidative stress and apoptosis in PC12 cells.
The neurotoxicity of fluoride is associated with oxidative stress due to imbalance between production and removal of reactive oxygen species (ROS). In contrast, induction of detoxifying and antioxidant genes through activation of NF-E2-related factor 2 (Nrf2) has been implicated in preventing oxidative stress and apoptosis in neurodegenerative diseases. The present
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
Co-exposure to Arsenic-Fluoride Results in Endoplasmic Reticulum Stress-Induced Apoptosis Through the PERK Signaling Pathway in the Liver of Offspring Rats.
Arsenic and fluoride are two of the major groundwater pollutants. To better understand the liver damage induced during development, 24 male rats exposed to fluoride (F), arsenic (As), and their combination (As + F) from the prenatal stage to 90 days after birth were selected for analysis. Histopathological results showed
Sodium Fluoride (NaF) Induces Inflammatory Responses Via Activating MAPKs/NF-kB Signaling Pathway and Reducing Anti-inflammatory Cytokine Expression in the Mouse Liver.
At present, no reports are focused on fluoride-induced hepatic inflammatory responses in human beings and animals. This study aimed to investigate the mRNA and protein levels of inflammatory cytokines and signaling molecules for evaluating the effect of different doses (0, 12, 24, and 48 mg/kg) of sodium fluoride (NaF) on inflammatory
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