Mechanism of mitochondrial transport of thallous ions.

Rat liver mitochondria were found to swell under nonenergized conditions when suspended in media containing 30-40 mM TINO3. Respiration on succinate caused a rapid contraction of mitochondria swollen under nonenergized conditions. In the presence of thallous acetate, there was a rapid initial swelling under nonenergized conditions until a plateau was reached; respiration on succinate then caused a further swelling. Trace amounts of 204Tl (less than 100 microM) equilibrated fairly rapidly across the mitochondrial membrane. The influx of Tl+ was able to promote the decay not only of a valinomycin-induced K+-diffusion potential but also of respiration-generated fields in the inner membrane in accordance with the electrophoretic nature of Tl+ movement. Efflux of Tl+ showed a half-time of about 10 sec at 20 degrees C and was not affected appreciably by the energy state. Efflux was retarded by Mg2+ and by lowering the temperature. The data indicate that Tl+ when present at high concentrations, 30mM or more, distributes across the mitochondrial inner membrane both in response to electrical fields and to delta pH. In energized mitochondria the uptake of Tl+ would occur electrophoretically, while Tl+/H+ exchange would constitute a leak. In the presence of NO3-, the movements of Tl+ are determined by that of NO3-, indicating short-range coupling of electrical forces. At low concentrations of Tl+, 5 mM or less, there was no indication of a Tl+/H+ exchange, which appears to be induced by high concentrations of Tl+.