Gramicidin induced ion transport in brain mitochondria preparations.

Abstract

Abstract— —(1) Gramicidin at low concentrations induces an uptake of K+ and Na+ in brain mitochondria in a manner similar to that observed with liver mitochondria.(2) The cation uptake is energy dependent, and is accompanied by an ejection of H+ ions and a slight increase in respiration in the absence of added permeant anion.(3) The cation uptake and hydrogen ion release are both inhibited by agents which inhibit electron transport. Barbiturates and chlorpromazine inhibit the transport phenomenon by inhibiting electron transport.(4) In the presence of permeant anions (phosphate and acetate) respiration is stimulated quite significantly.(5) At high gramicidin concentrations there is a release of Na+ and K+ from the mitochondria and uptake of H+. There is also a cyclic reduction‐oxidation of the nicotinamide adenine dinucleotides, which is believed to be due to the release from the mitochondria of the reduced dinucleotides followed by their subsequent oxidation.(6) The effect of high gramicidin on the mitochondrial nicotinamide‐adenine dinucleotides and cation distribution is irreversible and is not blocked by individual inhibitors of respiration and of phosphorylation, but is prevented by prior addition of a mixture of these inhibitors.(7) Gramicidin is therefore believed to have a bimodal function; one on the mitochondrial membrane per se, and the other on the energy dependent ion accumulation apparatus.(8) A model of induced mitochondrial ion accumulation is presented.