Membrane potential genesis in Nitella cells, mitochondria, and thylakoids.

The resting membrane potential of Nitella cells shifts in parallel with the change in H+ equilibrium potential, but is not equal to the H+ equilibrium potential. The deviation of the membrane potential from the H+ equilibrium potential depends on the extrusion rate of H+ by the electrogenic H+-pump. The activity of the electrogenic H+-pump was formulated in terms of the change in the free energy of ATP hydrolysis. The deviation of membrane potential from the H+ equilibrium potential induces a passive H+ flow. The passive inward H+ current may be coupled with Cl- uptake. The coupling rate of H+,Cl- co-transport was discussed. The membrane potential of mitochondria was electrochemically formulated in terms of oxidation-reduction H2/H+ half-cells spontaneously formed at the inner and outer boundaries of each trans-membrane electron-conducting pathway. The membrane potential formed by a pair of H2/H+ redox cells is pH-sensitive in its nature, but deviates from the H+ equilibrium potential to an extent that depends on the logarithm of the ratio of H2 concentrations at the inner and outer boundaries. The membrane potential of thylakoids is considered to be primarily due to the electromotive force of photocells embedded in the thylakoid membrane, as far as the anode and cathode of each photocell are in contact with the inner and outer solutions, respectively. The light-induced electronic current yields oxygen at the inner boundary and causes an increase in the H2 pool at the outer boundary of the electron-conducting pathway, which has no shunting plastoquinone chain between these two boundaries.