Bioenergetic aspects of apoptosis, necrosis and mitoptosis

Apoptosis. 2006 Apr;11(4):473-85. doi: 10.1007/s10495-006-5881-9.


In this review I summarize interrelations between bioenergetic processes and such programmed death phenomena as cell suicide (apoptosis and necrosis) and mitochondrial suicide (mitoptosis). The following conclusions are made. (I) ATP and rather often mitochondrial hyperpolarization (i.e. an increase in membrane potential, delta psi) are required for certain steps of apoptosis and necrosis. (II) Apoptosis, even if it is accompanied by delta psi and [ATP] increases at its early stage, finally results in a delta psi collapse and ATP decrease. (III) Moderate (about three-fold) lowering of [ATP] for short and long periods of time induces apoptosis and necrosis, respectively. In some types of apoptosis and necrosis, the cell death is mediated by a delta psi-dependent overproduction of ROS by the initial (Complex I) and the middle (Complex III) spans of the respiratory chain. ROS initiate mitoptosis which is postulated to rid the intracellular population of mitochondria from those that are ROS overproducing. Massive mitoptosis can result in cell death due to release to cytosol of the cell death proteins normally hidden in the mitochondrial intermembrane space.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adenosine Triphosphate / metabolism*
  • Apoptosis*
  • Energy Metabolism
  • Humans
  • Hydrogen Peroxide / metabolism
  • Membrane Potentials
  • Mitochondria / metabolism*
  • Mitochondria / ultrastructure
  • Mitochondrial Membranes / physiology
  • Necrosis*
  • Reactive Oxygen Species / metabolism
  • Saccharomyces cerevisiae / metabolism


  • Reactive Oxygen Species
  • Adenosine Triphosphate
  • Hydrogen Peroxide