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Selenite-induced apoptosis of osteoclasts mediated by the mitochondrial pathway

Youn Wook Chung1, Tae Soo Kim, Soo Young Lee

  • 1Laboratory of Cellular and Molecular Biochemistry, School of Life Sciences and Biotechnology, Korea University, Seoul.

Toxicology Letters
|August 23, 2005
PubMed

Insights

Sodium selenite triggers programmed cell death (apoptosis) in mature osteoclasts. This process involves the mitochondrial pathway and caspase-3 activation, offering insights into bone cell regulation.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Toxicology

Background:

  • Osteoclasts are crucial for bone resorption.
  • Understanding factors influencing osteoclast apoptosis is vital for bone health research.
  • Sodium selenite's effects on these cells are not fully elucidated.

Purpose of the Study:

  • To investigate the impact of sodium selenite on mature osteoclasts.
  • To elucidate the molecular mechanisms underlying selenite-induced osteoclast apoptosis.

Main Methods:

  • Osteoclast-like cells differentiated from RAW 264.7 cells were incubated with sodium selenite.
  • Apoptosis was assessed via morphological changes, DNA fragmentation, and caspase-3 activity.
  • Oxidative stress markers (superoxide anion, thiol groups), mitochondrial function (membrane potential, cytochrome c release), and pathway inhibitors were analyzed.

Main Results:

  • Sodium selenite induced apoptosis in osteoclast-like cells.
  • Selenite promoted oxidative stress, mitochondrial dysfunction, and caspase-3 activation.
  • Apoptosis was significantly inhibited by cyclosporin A and DEVD-CHO, implicating the mitochondrial permeability transition pore and caspase-3.

Conclusions:

  • Sodium selenite induces apoptosis in mature osteoclasts through the mitochondrial pathway.
  • The findings highlight selenite's role in regulating osteoclast viability and suggest potential therapeutic targets for bone diseases.

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