Abstract
Cytochrome c release from mitochondria to and subsequent accumulation in the cytosol has been considered a prerequisite for apoptosis. In this study, we present evidence for apoptosis induction without accumulation of cytochrome c in the cytosol. U937 lymphoma cells treated with staurosprine released cytochrome c from mitochondria to cytosol prior to PARP cleavage and DNA fragmentation. However, U937 cells treated with BMD188 (a hydroxamic acid and a potent apoptosis inducer) did not demonstrate any cytochrome c accumulation in the cytosol during apoptosis induction. This different pattern of cytochrome c alterations was also observed with these two inducers on leukemic HL60 cells and epithelial PC3 cells. Furthermore, when PC3 cells were treated with a panel of apoptosis-inducing agents, it was found that camptothecin, bleomycin, VP16 and TNF-α induced varying amounts of cytosolic accumulation of cytochrome c either prior to or concurrent with PARP cleavage while vinblastine and BHPP did not. Taken together, the present results suggest that cytochrome c accumulation in the cytosol during apoptosis is a cell type- and inducer-dependent phenomenon.
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