Modulation of the antioxidant defence as a factor in apoptosis

Research output: Contribution to journalArticle

78 Citations (Scopus)

Abstract

This review focuses on evidence that oxidative stress during apoptosis is controlled, at least in part, by modulating cellular antioxidant defences. Evidence is presented from studies of apoptosis induced by glucocorticoids, HIV-1 infection and tumour necrosis factor-α. Glucocorticoid treatment of murine lymphocyte cell lines leads to the down-regulation of primary antioxidant defence enzymes, including catalase, superoxide dismutases, thioredoxin and DT-diaphorase. Following HIV-1 infection, disturbances in glutathione metabolism are seen, and decreased antioxidant enzyme activities have been reported for HIV-1-infected cell lines. The viral protein Tat may mediate these effects. Cellular resistance to apoptosis induced by tumour necrosis factor-α is modulated by the expression of manganese superoxide dismutase or Bcl-2. The loss of antioxidant defences is predicted to lead to oxidative stress, which could contribute to the mechanism of apoptosis through an effect on redox-sensitive transcription factors, calcium homeostasis or cysteine proteases.

Original languageEnglish (US)
Pages (from-to)63-70
Number of pages8
JournalCell Death and Differentiation
Volume3
Issue number1
StatePublished - 1996

Fingerprint

Antioxidants
Apoptosis
HIV-1
Glucocorticoids
Superoxide Dismutase
HIV Infections
Oxidative Stress
Tumor Necrosis Factor-alpha
NAD(P)H Dehydrogenase (Quinone)
Cell Line
Thioredoxins
Cysteine Proteases
Viral Proteins
Enzymes
Catalase
Oxidation-Reduction
Glutathione
Homeostasis
Transcription Factors
Down-Regulation

Keywords

  • Glucocorticoids
  • HIV
  • Lymphocytes
  • Oxidative stress
  • Reactive oxygen species
  • TNF-α

ASJC Scopus subject areas

  • Cell Biology

Cite this

Modulation of the antioxidant defence as a factor in apoptosis. / Briehl, Margaret M; Baker, Amanda F.

In: Cell Death and Differentiation, Vol. 3, No. 1, 1996, p. 63-70.

Research output: Contribution to journalArticle

@article{180168b9b22948b8ac5127ad0d4a60b2,
title = "Modulation of the antioxidant defence as a factor in apoptosis",
abstract = "This review focuses on evidence that oxidative stress during apoptosis is controlled, at least in part, by modulating cellular antioxidant defences. Evidence is presented from studies of apoptosis induced by glucocorticoids, HIV-1 infection and tumour necrosis factor-α. Glucocorticoid treatment of murine lymphocyte cell lines leads to the down-regulation of primary antioxidant defence enzymes, including catalase, superoxide dismutases, thioredoxin and DT-diaphorase. Following HIV-1 infection, disturbances in glutathione metabolism are seen, and decreased antioxidant enzyme activities have been reported for HIV-1-infected cell lines. The viral protein Tat may mediate these effects. Cellular resistance to apoptosis induced by tumour necrosis factor-α is modulated by the expression of manganese superoxide dismutase or Bcl-2. The loss of antioxidant defences is predicted to lead to oxidative stress, which could contribute to the mechanism of apoptosis through an effect on redox-sensitive transcription factors, calcium homeostasis or cysteine proteases.",
keywords = "Glucocorticoids, HIV, Lymphocytes, Oxidative stress, Reactive oxygen species, TNF-α",
author = "Briehl, {Margaret M} and Baker, {Amanda F}",
year = "1996",
language = "English (US)",
volume = "3",
pages = "63--70",
journal = "Cell Death and Differentiation",
issn = "1350-9047",
publisher = "Nature Publishing Group",
number = "1",

}

TY - JOUR

T1 - Modulation of the antioxidant defence as a factor in apoptosis

AU - Briehl, Margaret M

AU - Baker, Amanda F

PY - 1996

Y1 - 1996

N2 - This review focuses on evidence that oxidative stress during apoptosis is controlled, at least in part, by modulating cellular antioxidant defences. Evidence is presented from studies of apoptosis induced by glucocorticoids, HIV-1 infection and tumour necrosis factor-α. Glucocorticoid treatment of murine lymphocyte cell lines leads to the down-regulation of primary antioxidant defence enzymes, including catalase, superoxide dismutases, thioredoxin and DT-diaphorase. Following HIV-1 infection, disturbances in glutathione metabolism are seen, and decreased antioxidant enzyme activities have been reported for HIV-1-infected cell lines. The viral protein Tat may mediate these effects. Cellular resistance to apoptosis induced by tumour necrosis factor-α is modulated by the expression of manganese superoxide dismutase or Bcl-2. The loss of antioxidant defences is predicted to lead to oxidative stress, which could contribute to the mechanism of apoptosis through an effect on redox-sensitive transcription factors, calcium homeostasis or cysteine proteases.

AB - This review focuses on evidence that oxidative stress during apoptosis is controlled, at least in part, by modulating cellular antioxidant defences. Evidence is presented from studies of apoptosis induced by glucocorticoids, HIV-1 infection and tumour necrosis factor-α. Glucocorticoid treatment of murine lymphocyte cell lines leads to the down-regulation of primary antioxidant defence enzymes, including catalase, superoxide dismutases, thioredoxin and DT-diaphorase. Following HIV-1 infection, disturbances in glutathione metabolism are seen, and decreased antioxidant enzyme activities have been reported for HIV-1-infected cell lines. The viral protein Tat may mediate these effects. Cellular resistance to apoptosis induced by tumour necrosis factor-α is modulated by the expression of manganese superoxide dismutase or Bcl-2. The loss of antioxidant defences is predicted to lead to oxidative stress, which could contribute to the mechanism of apoptosis through an effect on redox-sensitive transcription factors, calcium homeostasis or cysteine proteases.

KW - Glucocorticoids

KW - HIV

KW - Lymphocytes

KW - Oxidative stress

KW - Reactive oxygen species

KW - TNF-α

UR - http://www.scopus.com/inward/record.url?scp=0030051802&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030051802&partnerID=8YFLogxK

M3 - Article

C2 - 17180056

AN - SCOPUS:0030051802

VL - 3

SP - 63

EP - 70

JO - Cell Death and Differentiation

JF - Cell Death and Differentiation

SN - 1350-9047

IS - 1

ER -