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Activation of potassium-dependent H+ efflux from mitochondria by cadmium and phenylarsine oxide

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Abstract

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+ or PhAsO produces collapse of the ΔpH.

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Abbreviations

BAL:

British Anti-Lewisite or 2,3-dimercaptopropanol

2-ME:

2-mercaptoethanol

PhAsO:

phenylarsine oxide

FCCP:

carbonylcyanide trifluoromethoxyphenylhydrazone

HEPES:

N-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid

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Rao Sanadi, D., Hughes, J.B. & Joshi, S. Activation of potassium-dependent H+ efflux from mitochondria by cadmium and phenylarsine oxide. J Bioenerg Biomembr 13, 425–431 (1981). https://doi.org/10.1007/BF00743214

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  • DOI: https://doi.org/10.1007/BF00743214

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