We have studied the role of changes in mitochondrial membrane potential (ΔΨ) in two widely-used models of apoptosis, such as dexamethasone-treated rat thymocytes and U937 human cells treated with tumor necrosis factor-α and cycloheximide. To dissipate ΔΨ, we used low concentrations of valinomycin, unable per se to induce apoptosis, and demonstrated that the decline in ΔΨ exerts opposite effects in the two models. Indeed, in U937 cells, depolarization of mitochondria increased apoptosis, which decreased in rat thymocytes. This leads to the suggestion that disruption of ΔΨ plays opposite roles depending on the experimental model. In U937 cells, the drop of ΔΨ is a possible contributory cause for the apoptotic process; in rat thymocytes, it could be a limiting factor. We propose that these opposite effects could be due to the different ATP requirement of each apoptotic pathway. Copyright (C) 2000 Federation of European Biochemical Societies.
- Flow cytometry
- Mitochondrial membrane potential
ASJC Scopus subject areas
- Molecular Biology