Fluoride induces apoptosis in H9c2 cardiomyocytes via the mitochondrial pathway

Area of Science:

• Toxicology
• Cell Biology
• Cardiovascular Science

Background:

• Chronic excessive fluoride intake poses health risks, particularly to the cardiovascular system.
• High concentrations of fluoride can disrupt normal physiological functions.
• Understanding the cellular mechanisms of fluoride toxicity is crucial for public health.

Purpose of the Study:

• To investigate the mechanism of apoptosis induced by sodium fluoride (NaF) in H9c2 cells.
• To determine the toxic effects of varying NaF concentrations on cell proliferation and morphology.
• To elucidate the role of the mitochondrial pathway in NaF-induced cytotoxicity.

Main Methods:

• H9c2 cells were exposed to different concentrations of NaF for up to 96 hours.
• Cell proliferation, apoptosis, and morphological changes were assessed.
• Mitochondrial membrane potential and mRNA levels of apoptosis-related genes (caspase-3, caspase-9, cytochrome c) were measured.

Main Results:

• NaF inhibited H9c2 cell proliferation and induced significant morphological damage.
• Increased NaF concentrations led to higher rates of early apoptosis and decreased mitochondrial membrane potential.
• mRNA levels of caspase-3, caspase-9, and cytochrome c were elevated in a dose-dependent manner with NaF exposure.

Conclusions:

• Apoptosis is a key mechanism in sodium fluoride-induced toxicity in H9c2 cells.
• The mitochondrial pathway, involving caspase activation and cytochrome c release, is implicated in NaF-induced cell death.
• These findings underscore the potential cardiovascular risks associated with excessive fluoride exposure.