Abstract
NADH oxidation catalyzed by submitochondrial particles produced by sonic treatment (ETPH) is inhibited by N,N′-dicyclohexylcarbodiimide. The inhibition of electron-transfer activity is released by uncouplers of oxidative phosphorylation, but not by ADP nor by potassium or sodium ions, either in the presence or absence of valinomycin or tyrocidin. Low concentrations of potassium or sodium (0–30 mM) either in the presence or absence of valinomycin or tyrocidin do not significantly increase the rate of NADH oxidation by ETPH. High concentrations of sodium or potassium ions (30–120 mM) cause a significant increase in the rate of NADH oxidation by ETPH. It is suggested that the metal ion transport system is a property of the oriented inner mitochondrial membrane, and that high concentrations of metal ion are required to overcome the low permeability of the ETPH membrane in the inward direction in order to transport the metal ion actively in the outward direction.
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