GRAMICIDIN AND ION TRANSPORT IN ISOLATED LIVER MITOCHONDRIA

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Abstract
Gramicidin caused H+ production by liver mitochondria; this process was dependent on the presence of Na+, Li+, Rb+ or Cs+. In the presence of one of these alkali-metal ions and phosphate, gramicidin caused mitochondrial swelling and increased oxygen consumption. Uncoupling agents, anaerobic conditions or respiratory inhibitors both inhibited and reversed H+ production and swelling. Both these processes could be supported by coupled electron transport through even a restricted portion of the respiratory chain. NH4 + also caused stimulation of respiration in the presence of gramicidin. In this case phosphate was not required. NH4+, in the presence of gramicidin, caused contraction of the mitochondria and a reversal of K+-induced swelling and H+ production. Uncoupling agents or NH4+ together with gramicidin caused the release of Sr 2+ that had been accumulated by mitochondria in the presence of phosphate. These results are discussed in relation to a postulated respiration-dependent H+ pump located in the mitochondrial membrane. It is suggested that gramicidin allows alkali-metal ions to pass through the mitochondrial membrane.