MiP2005: Session 9

Abstract without presentation                                                 Mitochondrial Physiology Network 10.9: 109 (2005) - download pdf

 

Effect of thallium (I) ions on isolated rat liver mitochondria in the presence of nonactin.

Sergey M Korotkov, ER Nikitina, VV Glazunov

Sechenov Institute of Evolutionary Physiology and Biochemistry RAS, St.Petersburg; 194223 St.Petersburg, Thorez pr. 44, RU. - korotkov@SK1645.spb.edu

    It is known that the inner mitochondrial membrane is lightly permeable to Tl+ ions [1]. Transport of Tl+ in energized mitochondria occurs via the electrophoretic uniport mechanism [2,3]. It was found that nonactin being ionophore stimulates transport of Tl+ in mitochondrial matrix [3]. However, the mechanisms of effect of nonactin on mitochondria are not studied completely.

    Effects of Tl+ on isolated rat liver mitochondria were studied. Both uptake of 204Tl+ in the presence of various nonactin concentrations in a medium and action of Tl+-nonactin complex on uptake of 137Cs+ with valinomycin were tested in succinate-energized mitochondria. Besides, transport of Tl+ in mitochondria was evaluated from swelling of mitochondria incubated in the TlNO3 or Tl-acetate media. Action of Tl-acetate and nonactin on mitochondrial enzymes containing active SH-groups was estimated from their effects on the state 3, state 4, or 2,4-dinitrophenol uncoupled respiration of mitochondria.

    It was found that uptake of 204Tl+ by energized mitochondria was enhanced by an increase of nonactin concentration in the incubation medium. On the other hand, uptake of 137Cs+ by energized mitochondria was markedly decreased in the presence of Tl+ with nonactin in the medium. Nonactin accelerated swelling of nonenergized mitochondria in theTlNO3 medium. At the same time, contraction of mitochondria after their succinate energization was markedly retarded in the presence of nonactin. In the medium containing 25-50 mM Tl-acetate, swelling of mitochondria before and after succinate administration and mitochondrial contraction after oxygen depletion were accelerated in experiments with nonactin. The state 4 respiration of mitochondria in the Tl-acetate medium was 2.5-fold increased in the presence of nonactin. The state 3 or 2,4-dinitrophenol uncoupled mitochondrial respiration was not affected by nonactin. The problems of nonactin effects on active and passive transport of Tl+ across the inner mitochondrial membrane and importance of the transmembrane potential on the transport processes are discussed [4].

1.  Saris NE, Skulskii IA, Savina MV, Glasunov VV (1981) Mechanism of mitochondrial transport of thallous ions. J Bioenerg Biomembr. 13: 51-59.

2. Melnick RL, Monti LG, Motzkin SM (1976) Uncoupling of mitochondrial oxidative phosphorylation by thallium.Biochem. Biophys. Res. Commun. 69: 68-73.

3. Skulskii IA, Saris NE, Savina MV, Glasunov VV (1981) Uptake of thallous ions by mitochondria is stimulated by nonactin but not by respiration alone. Eur. J. Biochem. 120: 263-266.

4. Korotkov SM, Nikitina ER, Glazunov VV, Yagodina OV (2005) Effect of thallium ions on isolated mitochondria of rat liver in the presence of nonactin. Doklady Biochem. Biophys. 401: 97103.


to topPrint page

 
 

Mitochondrial Physiology