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Abstract
Bcl-2 inhibits most types of apoptotic cell death, implying a common mechanism of
lethality. Bcl-2 is localized to intracellular sites of oxygen free radical generation
including mitochondria, endoplasmic reticula, and nuclear membranes. Antioxidants
that scavenge peroxides, N-acetylcysteine and glutathione peroxidase, countered apoptotic
death, while manganese superoxide dismutase did not. Bcl-2 protected cells from H2O2-
and menadione-induced oxidative deaths. Bcl-2 did not prevent the cyanide-resistant
oxidative burst generated by menadione. Two model systems of apoptosis showed no increment
in cyanide-resistant respiration, and generation of endogenous peroxides continued
at an inherent rate that was unaltered by Bcl-2. Following an apoptotic signal, cells
sustained progressive lipid peroxidation. Overexpression of Bcl-2 functioned to suppress
lipid peroxidation completely. We propose a model in which Bcl-2 regulates an antioxidant
pathway at sites of free radical generation.