Abstract
The oxidative phosphorylation inhibitor DBCT (dibutylchloromethyltin chloride) inhibits state 3 respiration at a concentration less than that which stimulates K+ flux into respiring rat liver mitochondria. Inhibition of ADP-stimulated respiration by DBCT can be reversed or blocked by the dithiol 2,3-dimercaptopropanol. The data are consistent with previous suggestions that DBCT may interact with the ATP synthase via reaction with a dithiol group. The stimulation of K+ influx by DBCT is partially reversed by concentrations of 2-mercaptoethanol which fail to affect the inhibition of state 3 respiration by DBCT. The combination of DBCT plus 2,3-dimercaptopropanol inhibits mitochondrial K+ influx. The inhibitory effect of dicyclohexylcarbodiimide on K+ influx is not expressed in the presence of DBCT. Atractyloside has little effect on K+ influx in the presence or absence of DBCT. The combination of DBCT plus uncoupler induces a net loss of endogenous K+. Consideration is given to the alternative hypotheses that the acceleration of K+ influx by DBCT may involve either a direct link to the energy transduction apparatus, or may occur via separate activation of a passive transport mechanism.
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Abbreviations used: DBCT, dibutylchloromethyltin chloride; BAL, British Anti-Lewisite or 2,3-dimercaptopropanol;; 2-ME, 2-mercaptoethanol; DCCD, dicyclohexylcarbodiimide; DNP, 2,4-dinitrophenol.
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Diwan, J.J., DeLucia, A. & Rose, P.E. Interacting effects of dibutylchloromethyltin chloride, 2,3-dimercaptopropanol, and other reagents on mitochondrial respiration and K+ flux. J Bioenerg Biomembr 15, 277–288 (1983). https://doi.org/10.1007/BF00744525
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DOI: https://doi.org/10.1007/BF00744525