scholarly journals The stoichiometry of the exchange catalysed by the mitochondrial calcium/sodium antiporter

1985 ◽  
Vol 229 (1) ◽  
pp. 161-166 ◽  
Author(s):  
M D Brand
Keyword(s):  
Steady State ◽  
Thermodynamic Analysis ◽  
Rat Heart ◽  
Ruthenium Red ◽  
Heart Mitochondria ◽  
Mitochondrial Calcium ◽  
Ionophore A23187 ◽  
Obvious Change ◽  
Rat Heart Mitochondria

Rat heart mitochondria respiring on succinate in the presence of Ruthenium Red (to inhibit uptake on the Ca2+ uniporter) released Ca2+ on the calcium/sodium antiporter until a steady state was reached. Addition of the ionophore A23187 (which catalyses Ca2+/2H+ exchange) did not perturb this steady state. Thermodynamic analysis showed that if a Ca2+/nNa+ exchange with any value of n other than 2 was at equilibrium, addition of A23187 would cause an obvious change in extramitochondrial free [Ca2+]. Therefore the endogenous calcium/sodium antiporter of mitochondria catalyses electroneutral Ca2+/2Na+ exchange.

scholarly journals Electroneutral efflux of Ca2+ from liver mitochondria

1985 ◽  
Vol 225 (2) ◽  
pp. 413-419 ◽  
Author(s):  
M D Brand
Keyword(s):  
Steady State ◽  
Thermodynamic Analysis ◽  
Liver Mitochondria ◽  
Ruthenium Red ◽  
Ionophore A23187 ◽  
Measurable Change

Respiring liver mitochondria were allowed to export Ca2+ on the endogenous Ca2+/nH+ antiporter in the presence of Ruthenium Red (to inhibit uptake on the Ca2+ uniporter) until a steady state was reached. Addition of sufficient of the ionophore A23187 (which catalyses Ca2+/2H+ exchange) to bring the Ca2+ and H+ gradients into equilibrium did not alter the steady state. Thermodynamic analysis showed that if a Ca2+/nH+ exchange with any value of n other than 2 was at equilibrium, addition of A23187 would have caused an easily measurable change in extramitochondrial free [Ca2+]. Therefore, the endogenous carrier of liver mitochondria catalyses electroneutral Ca2+/2H+ antiport.

scholarly journals Role of calcium ions in the regulation of intramitochondrial metabolism. Effects of Na+, Mg2+ and ruthenium red on the Ca2+-stimulated oxidation of oxoglutarate and on pyruvate dehydrogenase activity in intact rat heart mitochondria

1980 ◽  
Vol 190 (1) ◽  
pp. 107-117 ◽  
Author(s):  
R M Denton ◽  
J G McCormack ◽  
N J Edgell
Keyword(s):  
Dehydrogenase Activity ◽  
Pyruvate Dehydrogenase ◽  
Rat Heart ◽  
Ruthenium Red ◽  
Heart Mitochondria ◽  
Heart Cells ◽  
Maximal Effect ◽  
Rat Heart Mitochondria ◽  
20 Nm

1. In uncoupled rat heart mitochondria, the kinetic parameters for oxoglutarate oxidation were very close to those found for oxoglutarate dehydrogenase activity in extracts of the mitochondria. In particular, Ca2+ greatly diminished the Km for oxoglutarate and the k0.5 value (concentration required for half-maximal effect) for this effect of Ca2+ was close to 1 microM. 2. In coupled rat heart mitochondria incubated with ADP, increases in the extramitochondrial concentration of Ca2+ greatly stimulated oxoglutarate oxidation at low concentrations of oxoglutarate, but not at saturating concentrations of oxoglutarate. The k0.5 value for the activation by extramitochondrial Ca2+ was about 20 nM. In the presence of either Mg2+ or Na+ this value was increased to about 90 nM, and in the presence of both to about 325 nM. 3. In coupled rat heart mitochondria incubated without ADP, increases in the extramitochondrial concentration of Ca2+ resulted in increases in the proportion of pyruvate dehydrogenase in its active non-phosphorylated form. The sensitivity to Ca2+ closely matched that found to affect oxoglutarate oxidation, and Mg2+ and Na+ gave similar effects. 4. Studies of others have indicated that the distribution of Ca2+ across the inner membrane of heart mitochondria is determined by a Ca2+-transporting system which is composed of a separate uptake component (inhibited by Mg2+ and Ruthenium Red) and an efflux component (stimulated by Na+). The present studies are entirely consistent with this view. They also indicate that the intramitochondrial concentration of Ca2+ within heart cells is probably about 2–3 times that in the cytoplasm, and thus the regulation of these intramitochondrial enzymes by Ca2+ is of likely physiological significance. It is suggested that the Ca2+-transporting system in heart mitochondria may be primarily concerned with the regulation of mitochondrial Ca2+ rather than cytoplasmic Ca2+; the possible role of Ca2+ as a mediator of the effects of hormones and neurotransmitters on mammalian mitochondrial oxidative metabolism is discussed.

scholarly journals Modulation of Ca2+ efflux from heart mitochondria

1979 ◽  
Vol 178 (3) ◽  
pp. 673-680 ◽  
Author(s):  
E J Harris
Keyword(s):  
Electron Microscope ◽  
Rat Heart ◽  
Time Lag ◽  
Nucleotide Binding ◽  
Ruthenium Red ◽  
Heart Mitochondria ◽  
Condensed State ◽  
Active Uptake ◽  
Rat Heart Mitochondria ◽  
Bongkrekic Acid

The efflux of Ca2+ from rat heart mitochondria has been examined by using Ruthenium Red to inhibit active uptake after predetermined loadings with Ca2+. The efflux is proportional to the internal Ca2+ load; it is increased by Na+ applied when the mitochondria are respiring and this effect is inhibited by oligomycin. The efflux of Ca2+ is diminished by ATP and by ADP, with the latter the more effective. Both active uptake and efflux of Ca2+ are slowed by bongkrekic acid; this action has a time lag. The lower efflux found with the nucleotides and with bongkrekic acid seems to correspond to the more condensed state seen in the electron microscope when these agents are applied [Stoner & Sirak (1973) J. Cell Biol. 56, 51-64, 65-73]. The results are discussed in relation to the less-permeable state being contingent upon nucleotide binding to the membrane.

scholarly journals Evidence that glucagon acts on the liver to decrease mitochondrial calcium stores

1983 ◽  
Vol 210 (1) ◽  
pp. 73-77 ◽  
Author(s):  
H M Baddams ◽  
L B F Chang ◽  
G J Barritt
Keyword(s):  
Steady State ◽  
Intact Cell ◽  
Isolated Hepatocytes ◽  
Ruthenium Red ◽  
Mitochondrial Calcium ◽  
Calcium Stores ◽  
Ionophore A23187 ◽  
Small Decrease ◽  
Significant Difference

1. Mitochondria isolated from rats treated with glucagon for 60 min or lives perfused in the presence of glucagon for 10 min exhibited lower rates of 45Ca2+ exchange than did control mitochondria when this was measured under steady-state conditions in the presence of Mg2+, ATP, Pi and 0.13 microM- or 0.16 microM-free Ca2+ at pH 7.4 and at 25 degrees C or 37 degrees C. Under these conditions no significant difference in the rates of Ruthenium Red-induced 45Ca2+ efflux was observed. These results contrast with earlier work in which mitochondria isolated from glucagon-treated livers were shown to exhibit faster rates of Ca2+ uptake [Yamazaki (1975) J. Biol. Chem. 250, 7924-7930] and slower rates of spontaneous Ca2+ efflux [Hughes & Barritt (1978) Biochem. J. 176, 295-304] when these parameters were measured under different incubation conditions, including supra-physiological concentrations of free Ca2+ and the absence of added Mg2+ and ATP. 2. Perfusion of livers with glucagon before the addition of adrenaline or the Ca2+-selective ionophore A23187, to release Ca2+ from intracellular stores, decreased the amount of Ca2+ released by these agents. 3. Incubation of isolated hepatocytes in the presence of glucagon at 1.3 mM extracellular Ca2+ induced a small decrease in the plateau of the 45Ca2+-exchange curve obtained under steady-state conditions. 4. It is concluded that the actions of glucagon on liver mitochondrial Ca2+ transporters lead to a decrease, rather than an increase, in mitochondrial Ca2+ stores in the intact cell.

Magnolol and honokiol isolated from magnolia officinalis protect rat heart mitochondria against lipid peroxidation

1994 ◽  
Vol 47 (3) ◽  
pp. 549-553 ◽  
Author(s):  
Yu-Chiang Lo ◽  
Teng Che-Ming ◽  
Chen Chieh-Fu ◽  
Chen Chien-Chih ◽  
Hong Chuang-Ye
Keyword(s):  
Lipid Peroxidation ◽  
Rat Heart ◽  
Heart Mitochondria ◽  
Rat Heart Mitochondria ◽  
Magnolia Officinalis

Involvement of SH-groups during interaction of diazoxide with the inner membrane of rat heart mitochondria

2007 ◽  
Vol 415 (1) ◽  
pp. 206-210 ◽  
Author(s):  
S. M. Korotkov ◽  
V. P. Nesterov ◽  
L. V. Emel’yanova ◽  
N. N. Ryabchikov
Keyword(s):  
Rat Heart ◽  
Heart Mitochondria ◽  
Inner Membrane ◽  
Sh Groups ◽  
Rat Heart Mitochondria

Abstract 104: Effects of Pinacidil and Ca 2 + on Sodium-loaded Rat Heart Mitochondria

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Sergey M Korotkov ◽  
Vladimir P Nesterov ◽  
Irina V Brailovskaya ◽  
Larisa V Emelyanova ◽  
Svetlana A Konovalova ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Rat Heart ◽  
Mitochondrial Membrane ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion ◽  
Potassium Acetate ◽  
Heart Mitochondria ◽  
Inner Mitochondrial Membrane ◽  
Rat Heart Mitochondria ◽  
Acetate Medium

Deterioration of the contractile parameters of the heart muscle caused by ischemia and followed reperfusion is known as the main postoperative complication which is related to Ca 2+ and Na + overload in cardiomyocytes and mitochondria. Pinacidil reduced the overload in ischemia/reperfusion experiments. The mechanism of this phenomenon is still not clear. We hypothesized that increased ion permeability of the inner mitochondrial membrane (IMM) followed drop of electrochemical potential (ΔΨ mito ) can reduce the calcium. The aim of the study was to elucidate the effect of pinacidil (100 μM) and Ca 2+ (100 μM ) on swelling, oxygen consumption and ΔΨ mito of isolated sodium-loaded rat heart mitochondria (RHM(Na)) energized glutamate and malate. Pinacidil significantly enchanced the permeability of IMM to protons in ammonium nitrate medium. Also increased swelling of RHM(Na) energized with substrates in potassium acetate medium revealed that pinacidil increased potassium transport into matrix. Pinacidil stimulated oxygen consumption of RHM(Na) in State 4 and detained Ca 2+ -induced dissipation of ΔΨ mito . Under condition of Ca 2+ and Na + overload simulating ischemia/reperfusion, RHM(Na) oxygen consumption was not affected with pinacidil in State 3 and in the presence of 2,4-dinitrophenol. Cyclosporin A and ADP, the inhibitors of mitochondrial permeability transition pore (MPTP), markedly decreased Ca 2+ - induced swelling of RHM(Na) in nitrate ammonium or potassium acetate medium in the presence of pinacidil. Carboxyatractyloside, an inhibitor of cytosolic side-specific adenine nucleotide translocase, eliminated a pinacidil-stimulated oxygen consumption of succinate-energized RHMNa in State 4 regardless of the presence of Ca 2+ . Pinacidil was also concluded to accelerat potassium flux into energized RHM(Na) and promot MPTP opening in the low conduction state. Based on our data we suggested that the effect of pharmacological preconditioning induced by pinacidil could be due to it’s direct effect on mitochondria which is connected with above stimulation of the potassium permeability of the inner mitochondrial membrane and following reduce of the ΔΨ mito that thus prevent calcium overload of cardiomyocytes after ischemia/reperfusion in turn.

Structure of paracrystalline arrays on outer membranes of rat-liver and rat-heart mitochondria

1992 ◽  
Vol 108 (3) ◽  
pp. 227-237 ◽  
Author(s):  
C.A. Mannella ◽  
A. Ribeiro ◽  
B. Cognon ◽  
D. D'Arcangelis
Keyword(s):  
Rat Liver ◽  
Rat Heart ◽  
Heart Mitochondria ◽  
Outer Membranes ◽  
Rat Heart Mitochondria
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