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Modulation of the antioxidant defence as a factor in apoptosis

M M Briehl1, A F Baker

  • 1Department of Pathology, University of Arizona, Tucson.

Cell Death and Differentiation
|January 1, 1996
PubMed

Insights

Cellular antioxidant defenses modulate oxidative stress during apoptosis. Impaired antioxidant enzymes and glutathione metabolism, seen in glucocorticoid treatment and HIV-1 infection, can promote programmed cell death.

Area of Science:

  • Cellular biology
  • Immunology
  • Biochemistry

Background:

  • Oxidative stress is implicated in apoptosis.
  • Cellular antioxidant defenses play a role in regulating this process.
  • Apoptosis can be induced by various stimuli including glucocorticoids, HIV-1, and tumor necrosis factor-alpha.

Purpose of the Study:

  • To review evidence on the modulation of cellular antioxidant defenses during apoptosis.
  • To explore the link between impaired antioxidant defenses and oxidative stress in apoptosis.
  • To examine specific examples of apoptosis induction and associated changes in antioxidant systems.

Main Methods:

  • Review of existing literature on apoptosis and oxidative stress.
  • Analysis of studies involving glucocorticoid-induced apoptosis in lymphocytes.
  • Examination of research on HIV-1 infection and its impact on antioxidant metabolism.
  • Investigation of tumor necrosis factor-alpha-induced apoptosis and resistance mechanisms.

Main Results:

  • Glucocorticoid treatment down-regulates key antioxidant enzymes like catalase and superoxide dismutases.
  • HIV-1 infection disrupts glutathione metabolism and decreases antioxidant enzyme activity, potentially mediated by the viral protein Tat.
  • Cellular resistance to tumor necrosis factor-alpha-induced apoptosis is influenced by manganese superoxide dismutase and Bcl-2 expression.

Conclusions:

  • Modulation of cellular antioxidant defenses is a key factor in controlling oxidative stress during apoptosis.
  • Loss of antioxidant defenses can lead to oxidative stress, contributing to apoptotic mechanisms.
  • Further research into redox-sensitive pathways is warranted to understand apoptosis regulation.

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