Induction of transmembrane proton transfer by mercurials in mitochondria. I. Ion movements accompanying transmembrane proton transfer.

The induction of energized proton release by mercurials in beef heart mitochondria appears to be mediated through the “activation” of an endogenous mitochondrial Na+/K+ ionophore. The effects of mercurials on mitochondria can be duplicated by the addition in their place of either purified mitochondrial Na+/K+ ionophore or a classical ionophorous species (e.g. gramicidin). Mitochondria which are submitted in turn to each of these three experimentally defined conditions acquire the capacity not only for energized proton release, but also for nonenergized proton uptake, nonenergized swelling in the presence of 0.10 M potassium or sodium chloride or nitrate in a sucrose-free medium, active transport of sodium or potassium acetate, and increased succinatedependent respiration. While such an extensive spectrum of near identical agent-activity relationships has led us to adopt the present thesis, more directly in support of the latter is the observation that the yield of ethanol-extractable Na+/ K+ ionophore from mitochondria is consistently increased upon pretreatment of mitochondria with mercurials such as fluorescein mercuric acetate.