Stimulation of K+ flux into mitochondria by phenylarsine oxide.
The dithiol-reactive reagent phenylarsine oxide causes a pH-dependent stimulation of unidirectional K+ flux into respiring rat liver mitochondria. This stimulation is diminished by subsequent addition of either the dithiol 2,3-dimercaptopropanol or the monothiol 2-mercaptoethanol. In contrast, uncoupling by phenylarsine oxide is reversed by 2,3-dimercaptopropanol but not by 2-mercaptoethanol. The data suggest separate sites of interaction of phenylarsine oxide with mechanisms of K+ entry and ATP synthesis. Stimulatory effects of mersalyl and phenylarsine oxide on K+ influx are not additive. Thus PheASO and mersalyl may affect K+ influx at a common site. Pretreatment of the mitochondria with DCCD, which inhibits K+ influx, fails to alter sensitivity to PheAsO or mersalyl. Thus the DCCD binding site associated with the K+ influx mechanism appears to be separate from and independent of the sulfhydryl group(s) which mediate stimulation of K+ influx by PheAsO and mersalyl. PheAsO, like mersalyl, also increases the rate of unidirectional K+ efflux from respiring mitochondria. The combined presence of PheAsO plus mersalyl causes a greater stimulation of K+ efflux than is observed with either reagent alone.
D000818:Animals; D001152:Arsenicals / Q000494:pharmacology*; D001693:Biological Transport, Active / Q000187:drug effects; D004024:Dicyclohexylcarbodiimide / Q000494:pharmacology; D007700:Kinetics; D008623:Mercaptoethanol / Q000494:pharmacology; D008634:Mersalyl / Q000494:pharmacology; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000378:metabolism*; D051381:Rats
D001152:Arsenicals; C029341:oxophenylarsine; D004024:Dicyclohexylcarbodiimide; D008634:Mersalyl; D008623:Mercaptoethanol; D011188:Potassium