Cytoplasmic acidification is not an effector mechanism of VP16 or DEX-induced apoptosis in CEM T leukaemia cells.
The role of intracellular acidification in the execution phase of apoptosis is not well understood. Here we examine the effect of Bcl-2 over-expression on intracellular acidification occurring during apoptosis. We found, that in CEM cells, neither DEX nor VP16-induced apoptosis lead to a significant change in intracellular pH (pHi). Furthermore, we found that shifting pHi away from physiological values was unable to induce chromatin condensation or poly(ADP-ribose) polymerase (PARP) cleavage in the presence of Bcl-2 over-expression. However, it was found that maximum chromatin condensation and PARP cleavage occurred at near physiological pHi values. Taken together these data suggest that intracellular acidification does not trigger the effector phase of CEM apoptosis.
D000143:Acids; D018931:Antineoplastic Agents, Hormonal / Q000378:metabolism* / Q000494:pharmacology; D017209:Apoptosis; D003593:Cytoplasm / Q000502:physiology; D003907:Dexamethasone / Q000378:metabolism* / Q000494:pharmacology; D005047:Etoposide / Q000378:metabolism* / Q000494:pharmacology; D006801:Humans; D006863:Hydrogen-Ion Concentration; D019384:Nucleic Acid Synthesis Inhibitors / Q000378:metabolism* / Q000494:pharmacology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D014407:Tumor Cells, Cultured