Effects of amyl ester of unsubstituted rhodamine on respiration and Ca2+ transport in rat liver mitochondria

Biochem Biophys Res Commun. 1991 Mar 29;175(3):1010-6. doi: 10.1016/0006-291x(91)91665-y.

Abstract

In rat liver mitochondria the amylrhodamine is responsible for uncoupling (respiratory stimulation in state 4) by two distinct processes. Immediately after amylrhodamine addition (2-12 microM) stimulation of respiration takes place. Respiration rate for this phase is constant in time, it is independent of the potassium or inorganic phosphate content in the medium, not inhibited by oligomycin, ruthenium red, cyclosporine A, N-ethyl-maleimide and EGTA. The second phase of the respiratory stimulation is not linear in time. Respiration rate within this phase increases with rising of potassium and phosphate content in the medium. This effect is abolished by oligomycin, ruthenium red, cyclosporine A, N-ethylmaleimide and EGTA. The beginning of respiratory increment coincides with the second phase of Ca2+ release from mitochondria.

MeSH terms

  • Animals
  • Biological Transport, Active / drug effects
  • Calcium / metabolism*
  • Cyclosporins / pharmacology
  • Egtazic Acid / pharmacology
  • Kinetics
  • Mitochondria, Liver / drug effects
  • Mitochondria, Liver / metabolism*
  • Oligomycins / pharmacology
  • Oxygen Consumption / drug effects*
  • Potassium / pharmacology
  • Rats
  • Rhodamines / pharmacology*
  • Ruthenium Red / pharmacology

Substances

  • Cyclosporins
  • Oligomycins
  • Rhodamines
  • Ruthenium Red
  • amyl rhodamine
  • Egtazic Acid
  • Potassium
  • Calcium