Abstract
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 of204Tl (less than 100 µM) 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°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, 30 mM or more, distributes across the mitochondrial inner membrane both in response to electrical fields and to Δ pH. In energized mitochondria the uptake of Tl+ would occur electrophoretically, while Tl+/H+ exchange would constitute a leak. In the presence of NO −3 , the movements of Tl+ are determined by that of NO −3 , 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+.
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Saris, NE.L., Skulskii, I.A., Savina, M.V. et al. Mechanism of mitochondrial transport of thallous ions. J Bioenerg Biomembr 13, 51–59 (1981). https://doi.org/10.1007/BF00744746
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DOI: https://doi.org/10.1007/BF00744746