Some effects of dibutylchloromethyltin chloride and other reagents on mitochondrial K+ flux.

Respiration-dependent K+ fluxes across the limiting membranes of isolated rat liver mitochondria, measured by means of 42K, are stimulated by the oxidative phosphorylation inhibitor dibutylchloromethyltin chloride (DBCT). A lack of effect of Cl- concentration indicates that the stimulation of K+ flux by DBCT is not attributable to Cl-/OH- exchange activity. The mercurial mersalyl was previously shown to stimulate respiration-dependent K+ influx. The combined presence of mersalyl plus DBCT results in a greater stimulation of K4 influx than is caused by either DBCT or mersalyl alone. The oxidative phosphorylation inhibitor oligomycin, which alone has no effect on respiration-dependent K+ influx, enhances the stimulatory effect of mersalyl on K+ influx. The data are consistent with, although not proof of, a direct interaction of the K+ transport mechanism with the mitochondrial energy transduction apparatus.