Cytoplasmic acidification is not an effector mechanism of VP16 or DEX-induced apoptosis in CEM T leukaemia cells

R. S P Benson, C. Dive, A. J M Watson

Research output: Contribution to journalArticlepeer-review

Abstract

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 DH (pH(i)). Furthermore, we found that shifting pH(i) 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 pH(i) values. Taken together these data suggest that intracellular acidification does not trigger the effector phase of CEM apoptosis.
Original languageEnglish
Pages (from-to)1755-1760
Number of pages5
JournalJournal of Cell Science
Volume112
Issue number11
Publication statusPublished - 1999

Keywords

  • Acidification
  • Apoptosis
  • bcl-2
  • CEM cells
  • Death
  • Flow cytometry

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