Cockerell, Harris and Pressman1 recently reported that when mitochondria which had been poisoned with rotenone were suspended in a potassium-free sucrose medium buffered with tris phosphate, the addition of valinomycin led to a rapid loss of potassium, a rapid but smaller uptake of hydrogen ions, and a simultaneous net synthesis of ATP. This synthesis of ATP, apparently at the expense of a downhill movement of potassium ions, is extremely interesting, but it may be interpreted in more than one way. Cockerell et al. compared the ATP synthesis in their experiments with the ATP synthesis which seems to accompany reversal of the “sod um pump” in the red cell membrane2, and suggest that the synthesis in mitochondria is similarly brought about by the reversal of an ATP-driven cation pump. The outward movement of potassium ions is, they suppose, directly coupled to ATP synthesis. This explanation may be correct, but it does require that a significant part of the efflux of potassium should take place through the pump pathway, and therefore—given that only the inner mitochondrial membrane serves as an effective barrier to small ions—valinomycin should act specifically at the pump sites, for example, by facilitating the access of potassium ions to those sites.
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GLYNN, I. Involvement of a Membrane Potential in the Synthesis of ATP by Mitochondria. Nature 216, 1318–1319 (1967). https://doi.org/10.1038/2161318a0
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