Activation of potassium-dependent H+ efflux from mitochondria by cadmium and phenylarsine oxide.
Addition of Cd2+ or phenylarsine oxide (PhAsO) to respiring rat liver mitochondria results first in acidification of the medium (H+ efflux) followed by disappearance of H+ (discharge of the pH gradient or uncoupling). The first phase of H+ efflux is dependent upon the presence of K+ in the medium, and is not seen in the presence of valinomycin, which is consistent with the conclusion that H+ efflux is linked to membrane potential-dependent uptake of K+. These effects are abolished by low levels of 2,3-dimercaptopropanol but potentiated by excess of 2-mercaptoethanol, showing involvement of a dithiol type of group in the response. Mersalyl produces only the H+ efflux, and subsequent addition of Cd2+ of PhAsO produces collapse of the delta pH.
D000818:Animals; D001152:Arsenicals / Q000494:pharmacology*; D001693:Biological Transport, Active / Q000187:drug effects; D002104:Cadmium / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D008623:Mercaptoethanol / Q000494:pharmacology; D008930:Mitochondria, Liver / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D012964:Sodium / Q000494:pharmacology
D001152:Arsenicals; D002104:Cadmium; C029341:oxophenylarsine; D008623:Mercaptoethanol; D012964:Sodium; D011188:Potassium