This review focuses on evidence that oxidative stress during apoptosis
is controlled, at least in part, by modulating cellular antioxidant d
efences. Evidence is presented from studies of apoptosis induced by gl
ucocorticoids, HIV-1 infection and tumour necrosis factor-alpha. Gluco
corticoid 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 decre
ased antioxidant enzyme activities have been reported for HIV-1-infect
ed cell lines. The viral protein Tat may mediate these effects. Cellul
ar resistance to apoptosis induced by tumour necrosis factor-alpha is
modulated by the expression of manganese superoxide dismutase or Bcl-2
. The loss of antioxidant defences is predicted to lead to oxidative s
tress, which could contribute to the mechanism of apoptosis through an
effect on redox-sensitive transcription factors, calcium homeostasis
or cysteine proteases.