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Mitochondria-targeted antioxidants do not prevent tumour necrosis factor-induced necrosis of L929 cells

Reagan M Jarvis1, Jana Göttert, Michael P Murphy

  • 1Department of Biochemistry, University of Otago, Dunedin, New Zealand.

Free Radical Research
|August 31, 2007
PubMed

Insights

Mitochondrial reactive oxygen species (ROS) are not essential for tumor necrosis factor (TNF)-induced cell death. Alternative mitochondrial functions, not ROS production, are critical for necrosis.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Toxicology

Background:

  • Mitochondrial reactive oxygen species (ROS) are implicated in tumor necrosis factor (TNF)-induced necrosis.
  • The role of mitochondrial ROS in TNF-induced necrosis requires further investigation.

Purpose of the Study:

  • To investigate the effect of mitochondria-targeted antioxidants on TNF-induced necrosis in L929 cells.
  • To explore the role of mitochondrial membrane potential uncoupling in TNF-induced necrosis.

Main Methods:

  • Treatment of L929 cells with TNF and various compounds.
  • Assessment of cell viability and necrosis.
  • Evaluation of mitochondrial membrane potential.

Main Results:

  • Lipid-soluble antioxidant BHA protected cells from TNF-induced necrosis.
  • Mitochondria-targeted antioxidants (MitoQ, MitoPBN) did not inhibit TNF-induced necrosis.
  • Mitochondrial uncouplers (FCCP, CCCP) inhibited TNF-induced necrosis in a dose-dependent manner.

Conclusions:

  • Mitochondrial ROS generation is not essential for TNF-induced necrosis.
  • Alternative mitochondrial functions, potentially respiration-dependent processes, are critical for necrotic cell death.

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