Mitochondrial protonophoric activity induced by a thyromimetic fatty acid analogue

Orit Hermesh, Bella Kalderon, Benjamin Berman, Jacob Bar-Tana*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

Calcium-dependent uncoupling of liver mitochondrial oxidative phosphorylation by a non-metabolizable long chain fatty acyl analogue was compared with uncoupling induced by in vivo thyroid hormone treatment. β,β'-Methyl-substituted hexadecane α,ω-dioic acid (Medica 16) is reported here to induce a saturable 20-30% decrease in liver mitochondrial ΔΨ, ΔpH and protonmotive force which proceeds in the presence of added Ca2+ to cyclosporin A-sensitive mitochondrial permeabilization. Ca2+-dependent uncoupling by Medica 16 was accompanied by atractylate-enhanced, bongkrekic-inhibited activation of mitochondrial Ca2+ efflux. The direct mitochondrial effect exerted in vitro by Medica 16 is similar to that induced by in vivo thyroid hormone treatment. Hence, the thyromimetic protonophoric activity of Medica 16 and the uncoupling activity of TH converge onto components of the mitochondrial permeabilization transition pore. Copyright (C) 2000 Elsevier Science B.V.

Original languageAmerican English
Pages (from-to)166-174
Number of pages9
JournalBiochimica et Biophysica Acta - Bioenergetics
Volume1457
Issue number3
DOIs
StatePublished - 21 Apr 2000

Keywords

  • Fatty acid
  • Mitochondria
  • Thyroid hormone
  • Uncoupling

Fingerprint

Dive into the research topics of 'Mitochondrial protonophoric activity induced by a thyromimetic fatty acid analogue'. Together they form a unique fingerprint.

Cite this