Magnesium and octylguanidinium inhibition of monovalent cation translocation in mitochondria.

G Beaty, C Gutiérrez, R López-Vancell, S Estrada

Index: Acta Physiol. Pharmacol. Latinoam. 36(3) , 217-32, (1986)

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Abstract

We have studied the inhibitory effects of several cations (OG+, Mg2+, Ca2+, Sr2+, Ba2+, Mn2+, La3+) on the uniport and exchange pathways for Na+ and K+ of rat liver mitochondria. Swelling of mitochondria suspended in sodium or potassium acetates indicates that: 1. Sodium passive influx to inhibited mitochondria is not affected by OG+ (in the microM range), and mM concentrations of polyvalent cations only induce a poor inhibition, the sequence being: La3+ greater than Mn2+ greater than Ca2+ greater than Mg2+ greater than Sr2+ = 0. 2. Sodium active influx is 50% inhibited by 60 microM Mg2+ or 90 microM OG+. La3+, Mn2+, Ca2+ and Sr2+ also inhibit Na+ influx (mM range). 10 mM Mg2+ or 35 microM OG+ are required to inhibit 50% K+ active influx. 3. Alkali cation efflux from partially swollen inhibited mitochondria is 50% blocked by 2 mM Mg2+ or 105 microM OG+ when sodium is the major permeable cation in the bathing solution. 3 mM Mg2+ or 3.8 microM OG+ are required for 50% inhibition when mitochondria are suspended in potassium acetate. 4. Alkali cation efflux from partially swollen respiring mitochondria suspended in sodium acetate is promoted by concentrations above 0.1-0.2 mM Mg2+ or 50-100 microM OG+. These data fit a mechanism including an energy-dependent Mg2+ and OG+ sensitive inward sodium translocator and a Mg2+ and OG+ insensitive cation/H+ exchanger working in dynamic balance.