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J. Biol. Chem., Vol. 265, Issue 14, 7837-7842, 05, 1990

Effects of the local anesthetic bupivacaine on oxidative phosphorylation in mitochondria. Change from decoupling to uncoupling by formation of a leakage type ion pathway specific for H+ in cooperation with hydrophobic anions

H Terada, O Shima, K Yoshida and Y Shinohara
Faculty of Pharmaceutical Sciences, University of Tokushima, Japan.

The effects of the local anesthetic bupivacaine on the oxidative phosphorylation in rat liver mitochondria were examined. Bupivacaine caused a maximum of about 7-fold stimulation of state 4 respiration at about 3 mM, released oligomycin-inhibited state 3 respiration, and activated ATPase to a similar extent to that by the weakly acidic uncoupler SF 6847. These effects were greatly enhanced by the addition of certain hydrophobic anions such as 1-anilino-8-naphthalenesulfonate, tetraphenyl borate, and picrate. In the absence of these anions, bupivacaine did not increase the proton conductance in either energized or nonenergized mitochondrial membranes or in artificial bilayer lipid membranes and did not have any effect on the proton motive force. However, it greatly enhanced the proton conductivity of these membrane systems and collapsed the proton motive force in the presence of hydrophobic anions. The results of noise analysis of artificial lipid bilayer membranes indicated that an ion pair complex of bupivacaine with hydrophobic anions formed a leakage-type ion pathway. Thus it is concluded that bupivacaine acts as a decoupler in the absence of added hydrophobic anions but in cooperation with certain anions as an uncoupler of oxidative phosphorylation due to formation of a H(+)- specific pathway in the membranes.
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