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.
D000818:Animals; D000968:Antimycin A / Q000494:pharmacology; D007425:Intracellular Membranes / Q000187:drug effects / Q000378:metabolism*; D008634:Mersalyl / Q000494:pharmacology; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D009840:Oligomycins / Q000494:pharmacology; D010085:Oxidative Phosphorylation / Q000187:drug effects; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D014220:Trialkyltin Compounds / Q000494:pharmacology*
D009840:Oligomycins; D014220:Trialkyltin Compounds; D008634:Mersalyl; C015129:dibutylchloro(chloromethyl)tin; D000968:Antimycin A; D011188:Potassium