1. 1. The effect on mitochondrial phosphate metabolism of glutamate and Pi, which energise K+ uptake, was compared with that of succinate and Pi, which do not. Glutamate induced a 3-fold increase in the turnover of ATP, as compared with succinate. The effect on phosphoprotein was even greater. 2. 2. K+-depleted mitochondria carried out oxidative phosphorylation at normal rates in the presence or absence of external K+. 3. 3. 2,4-Dinitrophenol caused K+ efflux from freshly prepared mitochondria. There was an equivalent H+ influx. This was due to an increase in permeability of the mitochondria to cations. Nupercaine decreased the change in permeability. 4. 4. 2,4-Dinitrophenol failed to induce H+ influx in mitochondria previously depleted of K+. H+ influx could also be decreased by balancing intramitochondrial K+ with equivalent concentrations of external K+, Na+ or NH4+ were less effective than K+. 5. 5. Oligomycin and amytal had no effect on mitochondrial permeability to cations. Azide had a lesser effect than 2,4-dinitrophenol. 6. 6. Oligomycin had no effect upon the K+ uptake energised by β-hydroxybutyrate, but blocked that energised by ATP.
Bibliographical noteFunding Information:
We are indebted to Miss S. ELSEY and Mr. W. GARRETT for skilled technical assistance. This work was supported by grants from the U.S. Public Health Service (AM 7226-o2), the Life Insurance Medical Research Fund, the Otho S. A. Sprague
Memorial Institute and the Burroughs-WellcomFeu nd. G.S.C. was in receipt of a travel grant: from the Anti Cancer Council, Victoria, Australia. A.E.M.McL. was in receipt of, a U.S. Public Health Service InternationalF ellowship.