Abstract

Highlights

• We studied the toxic effects of different concentrations of NaF in H9c2 cells.
• NaF inhibited H9c2 cell proliferation and induced early apoptosis.
• Mitochondrial membrane potential decreased with increase in NaF.
• Caspase-3, caspase-9, and cytochrome c mRNA levels increased with increase in NaF.
• Fluoride induces apoptosis via activation of the mitochondrial pathway.

Numerous studies have shown that chronic excessive fluoride intake can adversely affect different organ systems. In particular, the cardiovascular system is susceptible to disruption by a high concentration of fluoride. The objectives of this study were to explore the mechanism of apoptosis by detecting the toxic effects of different concentrations of sodium fluoride (NaF) in H9c2 cells exposed for up to 96 h. NaF not only inhibited H9c2 cell proliferation but also induced apoptosis and morphological damage. With increasing NaF concentrations, early apoptosis of H9c2 cells was increased while the mitochondrial membrane potential was decreased. Compared with the control group, the mRNA levels of caspase-3, caspase-9, and cytochrome c all increased with increasing concentrations of NaF. In summary, these data suggest that apoptosis is involved in NaF-induced H9c2 cell toxicity and that activation of the mitochondrial pathway may occur.

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