Fatty acid-induced Ca(2+)-dependent uncoupling and activation of external pathway of NADH oxidation are coupled to cyclosporin A-sensitive mitochondrial permeability transition. Academic Article uri icon

Overview

MeSH

  • Adenosine Diphosphate
  • Adenosine Triphosphate
  • Animals
  • Carnitine
  • Intracellular Membranes
  • Magnesium
  • Mitochondrial Swelling
  • Oxidation-Reduction
  • Oxygen Consumption
  • Palmitic Acid
  • Permeability
  • Rats

MeSH Major

  • Calcium
  • Cyclosporine
  • Mitochondria, Liver
  • NAD
  • Palmitic Acids

abstract

  • Permeabilization of inner mitochondrial membrane by palmitic acid in the presence of Ca2+ (cyclosporin A-sensitive stimulation of respiration, decrease of delta psi and high amplitude swelling) is accompanied by activation of the external pathway of NADH oxidation in liver mitochondria. The "pore"-sealing agents (cyclosporin A, Mg2+ with ADP, and L-carnitine with ATP) are equally effective in preventing the induction of external pathway of NADH oxidation by Ca2+ with palmitate. However, activities of these agents are different in respect to recoupling of permeabilized mitochondria. Participation of cyclosporin A-sensitive "pore" in the fatty acid- and Ca(2+)-dependent induction of external pathway of NADH oxidation and in Ca(2+)-dependent uncoupling is discussed.

publication date

  • April 1994

has subject area

  • Adenosine Diphosphate
  • Adenosine Triphosphate
  • Animals
  • Calcium
  • Carnitine
  • Cyclosporine
  • Intracellular Membranes
  • Magnesium
  • Mitochondria, Liver
  • Mitochondrial Swelling
  • NAD
  • Oxidation-Reduction
  • Oxygen Consumption
  • Palmitic Acid
  • Palmitic Acids
  • Permeability
  • Rats

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed ID

  • 8061632

Additional Document Info

start page

  • 1147

end page

  • 1155

volume

  • 32

number

  • 6