On the mechanism of rebounding of calcium in liver mitochondria.
Rat liver mitochondria are able to temporarily lower the steady state concentration of external Ca2+ after having accumulated a pulse of added Ca2+. This could be due to inhibition of efflux or/and stimulation of influx of Ca2+. This question has been addressed in mitochondria respiring on succinate +/- malonate. In the presence of malonate the depression of the membrane potential during Ca2+ uptake is more extensive and the rate of Ca2+ uptake slower. There were no discernible differences in the rates of efflux either after inhibition of the calcium uniporter by Ruthenium Red or by studying efflux of preloaded 45Ca-labeled Ca2+. The efflux was not changed by diltiazem or cyclosporin A to inhibit Ca2+ exchange on the Ca2+/nNA+ antiporter or efflux through the permeability transition pore. It is concluded that the rebounding is due mainly to stimulation of the calcium uniporter.
Saris
N E
NE
Department of Medical Chemistry, University of Helsinki, Finland.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels; D002135:Calcium-Binding Proteins / Q000378:metabolism*; D016572:Cyclosporine / Q000494:pharmacology; D004110:Diltiazem / Q000494:pharmacology; D007425:Intracellular Membranes / Q000187:drug effects / Q000378:metabolism; D008314:Malonates / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D008930:Mitochondria, Liver / Q000378:metabolism*; D010539:Permeability; D051381:Rats; D012430:Ruthenium Red; D019831:Sodium-Calcium Exchanger / Q000187:drug effects
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002135:Calcium-Binding Proteins; D008314:Malonates; D019831:Sodium-Calcium Exchanger; C034703:mitochondrial calcium uniporter; D012430:Ruthenium Red; D016572:Cyclosporine; C030290:malonic acid; D004110:Diltiazem; D002118:Calcium