The capacity of mitochondria isolated from
tumor cells to conserve the transmembrane electrochemical
proton gradient set up by respiration has been studied. In a K+ medium, mitochondria from
Ehrlich ascites tumor cells exhibit a capacity to conserve aerobic delta microH comparable to that displayed by normal rat liver mitochondria. Mitochondria from
Morris hepatoma 3924A show a decreased capacity to store delta microH+, which is principally due to lowering of delta pH. In a Na+ medium, both species of
tumor mitochondria show a significant decrease of aerobic delta pH, while delta psi is the same, with respect to rat liver mitochondria. Experiments on passive swelling show that mitochondria from
ascites tumor cells have an enhanced permeability to
chloride salts of
monovalent cations and increased activity of the Na+ (K+)-H+ exchange system of the mitochondrial membrane with respect to normal mitochondria. The enhanced activity of this system in
ascites cells is also shown by the characteristics of respiration-linked
proton translocation in submitochondrial particles and subsequent anaerobic
proton diffusion. It is concluded that the decreased capacity of mitochondria from
tumor cells to conserve aerobic delta pH is due to enhanced cyclic flow of Na+ across the membrane.