Chloride-dependent uncoupling mediated by oligomycin in rat liver mitochondria.

In rat liver mitochondria suspended in KCl medium and containing a low concentration of a K(+)-specific cationophore (valinomycin or Triton X-100), oligomycin was shown to induce uncoupling of oxidative phosphorylation, stimulation of adenosine triphosphatase activity, release of the respiratory control, decrease of energy-dependent changes in the fluorescence of the dye 8-anilino-1-naphthalenesulphonic acid and rapid swelling of mitochondria. Oligomycin caused none of the above effects when Br(-) or NO(3) (-) was substituted for Cl(-) as the major anionic species or when Na(+) replaced the K(+). The same concentration of oligomycin that caused uncoupling and swelling slightly improved energy-conserving reactions when the cationophores were omitted. In the presence of KSCN, valinomycin or Triton X-100 by itself caused uncoupling and swelling which was not further enhanced by oligomycin. On the basis of the above results it is suggested that the energy dissipation resulting from the concerted action of the cationophores and oligomycin is connected with the simultaneous transport of K(+) and its counter ion and that oligomycin plays its role in the uncoupling by facilitating the permeation of Cl(-) through the cristae membrane of the mitochondria.