Ba2+ uptake and the inhibition by Ba2+ of K+ flux into rat liver mitochondria.
Rapid uptake of Ba2+ by respiring rat liver mitochondria is accompanied by a transient stimulation of respiration. Following accumulation of Ba2+, e.g. at a concentration of 120 nmol per mg protein, the mitochondria exhibit reduced rates of state 3 and uncoupler-stimulated respiration. ADP-stimulated respiration is inhibited at a lower concentration of Ba2+ than is required to affect uncoupler-stimulated respiration, suggesting a distinct effect of Ba2+ on mechanisms involved in synthesis of ATP. Ba2+, which has an ionic radius similar to that of K+, inhibits unidirectional K+ flux into respiring rat liver mitochondria. This effect on K+ influx is observable at concentrations of Ba2+, e.g. 23 to 37 nmol per mg protein, which cause no significant change in state 4 or uncoupler-stimulated respiration. The accumulated Ba2+ decreases the measured Vmax of K+ influx, while having little effect on the apparent Km for K+. The inhibition of K+ influx by Ba2+ is seen in the presence and absence of mersalyl, an activator of K+ influx. In contrast, under the conditions studied, Ba2+ has no apparent effect on the rate of unidirectional K+ efflux. These data are consistent with the idea that K+ may enter and leave mitochondria via separate mechanisms.
D000818:Animals; D001464:Barium / Q000378:metabolism* / Q000494:pharmacology; D007700:Kinetics; D008634:Mersalyl / Q000494:pharmacology; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000378:metabolism*; D051381:Rats
D001464:Barium; D008634:Mersalyl; D011188:Potassium