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Potassium leakage during the apoptotic degradation phase
B Dallaporta1, T Hirsch, S A Susin
1Centre National de Recherche Scientifique, Villejuif, France.
Journal of Immunology (Baltimore, Md. : 1950)
|May 30, 1998
Summary
Potassium (K+) outflow is a key event in apoptosis, occurring after mitochondrial dysfunction but before DNA fragmentation. This K+ loss is crucial for triggering DNA degradation during programmed cell death.
Area of Science:
- Cell Biology
- Biochemistry
- Immunology
Background:
- Apoptosis involves significant cellular changes, including ion flux.
- The role of specific ion disruptions, like potassium (K+), in apoptosis is not fully understood.
Purpose of the Study:
- To investigate the impact of K+ outflow on apoptosis in thymocytes and T cell hybridoma cells.
- To determine the timing and necessity of K+ loss in the apoptotic cascade.
Main Methods:
- Single-cell analysis using K+-sensitive fluorochrome benzofuran isophtalate.
- Inhibition of mitochondrial transmembrane potential loss using Bcl-2, bongkrekic acid, and cyclosporin A.
- Assessment of phosphatidylserine exposure, glutathione levels, reactive oxygen species, Ca2+ influx, and DNA fragmentation.
Main Results:
- Significant K+ outflow was observed during apoptosis, irrespective of the death stimulus.
- K+ loss is dependent on the disruption of the inner mitochondrial transmembrane potential.
- K+ outflow precedes DNA fragmentation and is required for chromatinolysis in a cell-free system.
Conclusions:
- K+ outflow is a critical, early event in apoptosis, linked to mitochondrial dysfunction.
- Disruption of K+ homeostasis plays a vital role in apoptotic degradation and DNA fragmentation.
- Low K+ concentrations may derepress endonucleases, facilitating DNA fragmentation.