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A decrease in intracellular glutathione concentration precedes the onset of apoptosis in murine thymocytes

J P Beaver1, P Waring

  • 1Division of Cell Biology, John Curtin School of Medical Research, Australian National University, Canberra/Australia.

European Journal of Cell Biology
|September 1, 1995
PubMed
Summary

Cellular oxidant defense systems, particularly glutathione (GSH) levels, play a crucial role in triggering apoptosis. Changes in intracellular glutathione status, not just loss, appear to initiate programmed cell death.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Immunology

Background:

  • Free radical damage is linked to apoptosis induction.
  • The role of the cell's oxidant defense system in apoptosis signaling remains unclear.

Purpose of the Study:

  • To investigate if the cell's oxidant defense system status influences apoptosis signaling pathways.
  • To determine the role of intracellular glutathione (GSH) and oxidized glutathione (GSSG) in apoptosis.

Main Methods:

  • Induction of apoptosis in mouse thymocytes using dexamethasone, thapsigargin, and gliotoxin.
  • Measurement of apoptosis via propidium iodide DNA staining.
  • Assessment of intracellular glutathione ([GSH]i) levels.

Main Results:

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  • A correlation was observed between apoptosis percentage and lowered [GSH]i across all stimuli.
  • Reduced glutathione inhibited dexamethasone-induced apoptosis and the associated rise in lowered [GSH]i.
  • Oxidized glutathione treatment led to high levels of apoptosis, suggesting it's not solely GSH loss.

Conclusions:

  • A decrease in [GSH]i, an increase in [GSSG]i, or altered [GSH]i/[GSSG]i ratio may trigger apoptosis.
  • The oxidant defense system is integral to the signaling pathways initiating programmed cell death.
  • Glutathione redox state is a critical factor in regulating thymocyte apoptosis.