Effects of the membrane potential upon the Ca(2+)- and cumene hydroperoxide-induced permeabilization of the inner mitochondrial membrane

FEBS Lett. 1991 Dec 16;295(1-3):77-80. doi: 10.1016/0014-5793(91)81389-p.

Abstract

A protonophore-induced delta psi decrease in a 180-140 mV range causes an increase in the lag-period of Ca(2+)-induced mitochondrial permeabilization but has little effect on the cumene hydroperoxide-induced permeability transition of mitochondria. Suppression of the non-specific permeability induction seems to be mediated by an increase in [ADP] in the mitochondrial matrix. A further decrease in delta psi leads to additional suppression of the non-specific permeability as a result of a partial ruthenium red-sensitive efflux of the previously accumulated Ca2+. On the other hand, complete dissipation of delta psi causes immediate induction of the non-specific permeability. It is concluded that only complete dissipation of delta psi caused by H+ leakages may act as a trigger for non-specific permeability induction.

MeSH terms

  • Animals
  • Atractyloside / analogs & derivatives
  • Atractyloside / pharmacology
  • Benzene Derivatives / pharmacology*
  • Calcium Chloride / pharmacology*
  • Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / pharmacology
  • Intracellular Membranes / drug effects
  • Intracellular Membranes / physiology*
  • Kinetics
  • Membrane Potentials / drug effects
  • Mitochondria, Liver / drug effects
  • Mitochondria, Liver / physiology*
  • Mitochondrial Swelling / drug effects
  • Permeability
  • Rats
  • Ruthenium Red / pharmacology
  • Submitochondrial Particles / drug effects
  • Submitochondrial Particles / physiology*

Substances

  • Benzene Derivatives
  • Ruthenium Red
  • Atractyloside
  • Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone
  • Calcium Chloride
  • cumene hydroperoxide
  • carboxyatractyloside