Abstract
Abstract The energy-linked transport of K+ and other monovalent cations in isolated heart mitochondria is markedly activated by p-chloromercuriphenylsulfonate (CMS) and other mercurial reagents. The accumulation is supported by either respiration or exogenous ATP and is accompanied by reversible swelling. Respiration with physiological substrates is initially activated by CMS but becomes severely inhibited as the reaction proceeds. Sustained cation accumulation can be obtained with ascorbate and N,N,N',N'-tetramethylphenylenediamine as substrate. The energy-linked uptake of Li+, Na+, and other cations also appears to be activated by CMS. Maximum response is obtained in the presence of K+ and Li+, however. The activated accumulation of K+ can be abolished by the addition of cysteine and delayed by EDTA. We have previously reported that Zn++ and other heavy metal cations produce an activation of K+ accumulation similar to that seen with CMS. Zn++ added in addition to CMS produces enhanced uptake of K+ and swelling under most conditions, but the synergistic effect of the two reagents depends on the order of addition and the composition of the suspending medium. The effects of Zn++ are enhanced in media containing phosphate whereas those of CMS are inhibited by Pi. The amount of CMS which reacts with the membrane under the conditions of activated cation uptake depends on the concentration of CMS and the time of reaction. CMS uptake corresponding to about 10 to 20 mµmoles of fast reacting thiol groups results in maximum activation of monovalent cation uptake. The bulk of the total mitochondrial thiol groups are not available to the mercurial under the conditions of activated ion uptake. The reaction of mercurials with the mitochondrial membrane can be reversed by cysteine, and under these conditions the activated rate of swelling and ion uptake is inhibited.
Published Version
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