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Alkali ion complex formation by the cyclic depsipeptide, valinomycin, has been studied by means of nuclear magnetic resonance spectroscopy. Characteristic perturbations of the positions and fine structures of the resonances of the protons of specific groups were observed upon complextion of the valinomycin with KCNS and CsCNS in CDCI3. Small amounts of water did not affect the structure of the complexes as judged by nuclear magnetic resonance spectral criteria. Preliminary studies were carried out on the rates of complexation and decomplexation using the broadening of the lactate methyl proton resonances. A measurable rate of transfer of the complexed cation between valinomycin molecules in 80% CH3OH, 20% CDCl3, was observed while no measurable exchange rate was observed in pure CDCl3. These results are consistent with valinomycin functioning as a mobile ion carrier in biological membrane systems.

The glucose-induced increase in light scattered by Ehrlich ascites cells has been ascribed by Packer and Golder to a decrease in mitochondrial volume. They further suggest that the parallel inhibition of respiration and glycolysis arises from the inability of ATP to escape from such contracted mitochondria. We find that the glucose-induced light scattering changes occur not only in the presence of oligomycin, which prevents ATP formation (exclusive of substrate level phosphorylation), but that the same scattering changes are induced by this antibiotic alone. Other mitochondrial inhibitors, such as antimycin A and uncoupling agents, increase light scattering of the tumor cells. Valinomycin, which induces a specific volume change of mitochondria associated with the uptake of K+, causes a large decrease of scattering signal from ascites cells, even in the presence of glucose. As is the case with isolated mitochondria, this swelling is reversed by depletion of mitochondrial energy reserves, by uncoupling, or by anaerobiosis. It is concluded that the light scattering changes obtained with ascites cells during altered metabolic states indeed reflect mitochondrial changes, but the glucose-induced increase in light scattering is not a consequence of the inability of ATP to escape from the mitochondria. The only point in common for a wide variety of agents including glucose which induce a mitochondrial contraction is their ability to lower the mitochondrial energy reserves.