Inhibition of receptor-mediated apoptosis upon Bcl-2 overexpression is not associated with increased antioxidant status. 
Bcl-2 is reported to augment the antioxidant capacity of cells and this is hypothesized to contribute to the anti-apoptotic activity of this oncoprotein.  We generated a number of stable Jurkat cell lines expressing varying levels of Bcl-2, and showed a strong correlation between Bcl-2 levels and resistance to Fas-mediated apoptosis.  While individual differences could be detected, there was no overall correlation between Bcl-2 and the expression and activity of superoxide dismutases, catalase, glutathione peroxidases, thioredoxin, thioredoxin reductases, and peroxiredoxins.  Cells transfected with Bcl-2 averaged 70% more glutathione than parental cells, but there was no correlation between glutathione and resistance to apoptosis.  This challenges the hypothesis that the anti-apoptotic properties of Bcl-2 are linked to a global increase in antioxidant status.