On the Role of K+ on Oxidative Phosphorylation

Abstract

Abstract The influence of K+ on oxidative phosphorylation of rat liver mitochondria has been investigated. Fresh mitochondria undergo a loss of respiratory control concomitantly with the loss of K+, and a rough correlation was found between the K+ content of the mitochondria and the State 3 to State 4 respiratory ratio. K+-depleted mitochondria have a low respiratory control with NAD-dependent substrates which is significantly enhanced by adding K+ during State 4; K+, added during State 3, fails to affect respiration. Apparently, the respiratory response of the mitochondria to the cation is regulated by its metabolic state. The favorable effect of K+ on oxidative phosphorylation is independent of its action in promoting the entrance of oxidizable substrates into the mitochondria. In K+-depleted mitochondria, there are certain conditions in which valinomycin, but not 2,4-dinitrophenol, stimulates the respiratory activity. As evidenced by swelling experiments, valinomycin induces the passive entrance of K+ into the K+-depleted mitochondria. The results of an attempt to determine the distribution of K+ in the population of mitochondria which have been depleted of K+ suggest that a significant part of the population has extremely low levels of K+, whereas a small part has an adequate concentration of K+. The favorable effect of K+ on mitochondrial respiration is not specific, and other cations, except Na+, may substitute for K+. The order of effectiveness of the cations in inducing respiratory control in K+-depleted mitochondria follows the order by which cations alter the structure of macromolecules.