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Apoptosis is induced by decline of mitochondrial ATP synthesis in erythroleukemia cells

Marina Comelli1, Francesca Di Pancrazio, Irene Mavelli

  • 1Department of Biomedical Sciences and Technologies, University of Udine, Italy. mcomelli@dstb.uniud.it

Free Radical Biology & Medicine
|April 23, 2003
PubMed

Insights

Impaired mitochondrial ATP synthesis and energy charge are early events triggering apoptosis in erythroleukemia cells. This occurs regardless of whether the trigger is a mitochondrial ATP synthase inhibitor or oxidative stress.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Cancer Research

Background:

  • Apoptosis, or programmed cell death, is crucial for development and disease.
  • Mitochondrial dysfunction is implicated in various pathologies, including cancer.
  • Erythroleukemia cells offer a model to study apoptosis induction.

Purpose of the Study:

  • To investigate the role of mitochondrial ATP synthase inhibition in apoptosis.
  • To explore the mechanism of hydrogen peroxide-induced apoptosis in erythroleukemia cells.
  • To identify common early events in apoptosis execution.

Main Methods:

  • Incubation of erythroleukemia cells with oligomycin to inhibit mitochondrial ATP synthase.
  • Exposure of differentiation-induced erythroleukemia cells to hydrogen peroxide (H(2)O(2)).
  • Measurement of cellular ATP content, energy charge, mitochondrial respiration, DNA fragmentation, and plasma membrane integrity.

Main Results:

  • Oligomycin treatment led to early decline in energy charge and ATP, decreased respiration, and delayed DNA fragmentation and membrane damage.
  • Hydrogen peroxide exposure in iron-overloaded cells also impaired energy charge and induced apoptosis.
  • Hydroxyl radicals (*)OH generated by iron-catalyzed reactions were implicated in H(2)O(2)-induced apoptosis.

Conclusions:

  • Impairment of mitochondrial ATP synthesis and cellular energy charge are critical early events in apoptosis.
  • This mechanism is conserved across different apoptotic stimuli, including direct ATP synthase inhibition and oxidative stress.
  • Mitochondrial bioenergetics disruption plays a key role in apoptosis execution in erythroleukemia cells.

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