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Sodium fluoride induces apoptosis and alters bcl-2 family protein expression in MC3T3-E1 osteoblastic cells

Shiyong Yang1, Zhi Wang, Colin Farquharson

  • 1College of Veterinary Medicine, China Agricultural University, 100193 Beijing, China.

Biochemical and Biophysical Research Communications
|June 29, 2011
PubMed

Insights

Excessive fluoride (NaF) exposure harms osteoblasts, reducing cell viability and increasing apoptosis by altering bcl-2 and bax expression. This study clarifies fluoride

Area of Science:

  • Cell Biology
  • Toxicology
  • Biochemistry

Background:

  • Chronic excessive fluoride intake can cause fluorosis and bone pathologies.
  • The cellular mechanisms of sodium fluoride (NaF)-induced cytotoxicity in osteoblasts remain unclear.

Purpose of the Study:

  • To investigate the effects of NaF on osteoblastic cell viability, cell cycle, apoptosis, and bcl-2 family member expression.
  • To elucidate the cellular mechanisms of fluoride toxicity in osteoblasts.

Main Methods:

  • MC3T3-E1 osteoblastic cells were treated with varying concentrations of NaF (10⁻⁵ to 10⁻³ M) for up to 48 hours.
  • Cell viability, cell cycle progression, apoptosis, and the expression of bcl-2 and bax (mRNA and protein levels) were analyzed.

Main Results:

  • NaF reduced osteoblast cell viability in a dose- and time-dependent manner.
  • NaF induced apoptosis even at low concentrations, associated with decreased bcl-2/bax ratio.
  • NaF treatment caused S-phase arrest in the cell cycle and altered bcl-2 family gene expression.

Conclusions:

  • Fluoride-induced osteoblast apoptosis is mediated by direct effects on bcl-2 family member expression.
  • NaF cytotoxicity involves apoptosis and cell cycle disruption in osteoblasts.

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