Protection of hepatocytes against death due to mitochondrial failure: effect of di-Calciphor on antimycin A-induced toxicity

Toxicol Appl Pharmacol. 1994 May;126(1):33-8. doi: 10.1006/taap.1994.1087.

Abstract

Di-Calciphor is a synthetic derivative of prostaglandin B1 that protects against cerebral and cardiac ischemia apparently by preserving mitochondrial function. To determine whether di-Calciphor specifically protects against mitochondrial failure, we studied its effects on mitochondrial functions in hepatocytes treated with the specific mitochondrial poison, antimycin A. The results show that 1 microM di-Calciphor protects against cell death at concentrations of antimycin A that inhibited mitochondrial respiration and caused cellular ATP depletion. Di-Calciphor did not protect against loss of ATP but did protect against the loss of mitochondrial delta psi and delta pH. In addition, di-Calciphor protected against antimycin A-induced loading of phosphate into mitochondria and an associated mitochondrial swelling. Thus, these results show that di-Calciphor protects against a specific mitochondrial poison and support the interpretation that di-Calciphor is a mitochondrial protective agent. In addition, the results suggest that the protection of the mitochondria involves preservation of mitochondrial ionic and osmotic stability and does not involve improved ATP supply.

Publication types

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

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Animals
  • Antimycin A / antagonists & inhibitors*
  • Antimycin A / toxicity*
  • Cell Death / drug effects
  • In Vitro Techniques
  • Liver / cytology
  • Liver / drug effects*
  • Liver / metabolism
  • Male
  • Membrane Potentials / drug effects
  • Mitochondria, Liver / drug effects*
  • Phosphates / metabolism
  • Prostaglandins B / pharmacology*
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Phosphates
  • Prostaglandins B
  • di-Calciphor
  • Antimycin A
  • Adenosine Triphosphate