Mechanism of sodium ion independent calcium ion efflux from rat liver mitochondria

Biochemistry ◽  
1983 ◽  
Vol 22 (26) ◽  
pp. 6341-6351 ◽  
Author(s):  
T. E. Gunter ◽  
J. H. Chace ◽  
J. S. Puskin ◽  
K. K. Gunter
Keyword(s):  
Rat Liver ◽  
Calcium Ion ◽  
Liver Mitochondria ◽  
Sodium Ion ◽  
Rat Liver Mitochondria ◽  
Ion Efflux

scholarly journals The nature of the calcium ion efflux induced in rat liver mitochondria by the oxidation of endogenous nicotinamide nucleotides

1980 ◽  
Vol 188 (1) ◽  
pp. 113-118 ◽  
Author(s):  
D G Nicholls ◽  
M D Brand
Keyword(s):  
Membrane Potential ◽  
Rat Liver ◽  
Calcium Ion ◽  
Respiratory Control ◽  
Liver Mitochondria ◽  
Critical Value ◽  
Mitochondrial Damage ◽  
Rat Liver Mitochondria ◽  
Ion Efflux ◽  
Complete Collapse

Ca2+ efflux from rat liver mitochondria can occur when endogenous nicotinamide nucleotides are oxidized. It is suggested that nicotinamide nucleotide induced by acetoacetate sensitizes the mitochondria to damaage resulting from the accumulation of Ca2+ in the presence of Pi. Thus, acetoacetate-induced Ca2+ efflux is associated with a loss of respiratory control. Both the effluxes induced by acetoacetate and by high Ca2+ accumulation are prevented by ATP plus oligomycin, although these agents do not prevent the endoagenous nicotinamide nucleotides from becoming oxidized on addition of acetoacetate. Acetoacetate addition only results in Ca2+ release if the Ca2+ and Pi concentration are above a critical value. The acetoacetate-induced Ca2+ effflux is exactly paralled by the virtually complete collapse of the membrane potential. The presence of acetoacetate decreases the concentration of total Ca2+ necessary to induced mitochondrial damage by about 130 nmol of Ca2+/mg of protein. It is concluded that acetoacetate-induced efflux occurs by reversal of the Ca2+ uniporter after the collapse of the membrane potential.

scholarly journals Effect of micromolar concentrations of manganese ions on calcium-ion cycling in rat liver mitochondria

1983 ◽  
Vol 212 (3) ◽  
pp. 773-782 ◽  
Author(s):  
B P Hughes ◽  
J H Exton
Keyword(s):  
Rat Liver ◽  
Calcium Ion ◽  
Incubation Medium ◽  
Liver Mitochondria ◽  
Ruthenium Red ◽  
Rat Liver Mitochondria ◽  
Manganese Ions ◽  
Dose Dependent Decrease ◽  
Incubation Temperatures ◽  
Dose Dependent

The effects of micromolar concentrations of Mn2+ on the rat liver mitochondrial Ca2+ cycle were investigated. It was found that the addition of Mn2+ to mitochondria which were cycling 45Ca2+ led to a rapid dose dependent decrease in the concentration of extramitochondrial 45Ca2+ of about 1 nmol/mg of protein. The effect was complete within 30 s, was half maximal with 10 microM Mn2+ and was observed in the presence of 3 mM Mg2+ and 1 mM ATP. It occurred over a broad range of incubation temperatures, pH and mitochondrial Ca2+ loads. It was not observed when either Mg2+ or phosphate was absent from the incubation medium, or in the presence of Ruthenium Red. These findings indicate that micromolar concentrations of Mn2+ stimulate the uptake of Ca2+ by rat liver mitochondria, and provide evidence for an interaction between Mg2+ and Mn2+ in the control of mitochondrial Ca2+ cycling.

scholarly journals Calcium ion-induced uptakes and transformations of substrates in liver mitochondria

1969 ◽  
Vol 115 (4) ◽  
pp. 645-652 ◽  
Author(s):  
E J Harris ◽  
Celia Berent
Keyword(s):  
Energy Source ◽  
Rat Liver ◽  
Calcium Ion ◽  
Control Mechanism ◽  
Energy Requirement ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Carboxyl Group ◽  
Anionic Charge ◽  
Cellular Control

Substrate-depleted rat liver mitochondria will reaccumulate malate, succinate, oxoglutarate, β-hydroxybutyrate and glutamate if provided with an energy source and Ca2+ (or Ca2+ and Mn2+). The energy requirement for ion uptake by fresh mitochondria causes a transient oxidation of their NADH and presumably this leads to an increased oxaloacetate concentration. A consequence is the promotion of formation of citrate, which tends to remain in the particles, provided the pH is above 7. Analyses made of systems blocked with fluorocitrate show that citrate accumulates when Ca2+ is added with the following substrates; (a) pyruvate in the presence of ATP or malate, (b) palmitoyl-l(−)-carnitine in presence of malate and (c) oxoglutarate. Lowering the pH, even to 6·8, causes the citrate to emerge. This could be the basis of a cellular control mechanism. The generation of citrate in response to Ca2+ can explain the stoichiometry of one proton ejected per Ca2+ ion taken up. The new carboxyl group formed from acetyl-CoA when it condenses with oxaloacetate provides an internal anionic charge and a proton to emerge when Ca2+ enters.

scholarly journals SOME PERMEABILITY PROPERTIES OF ISOLATED RAT LIVER CELL MITOCHONDRIA

1956 ◽  
Vol 40 (1) ◽  
pp. 47-71 ◽  
Author(s):  
Kenneth L. Jackson ◽  
Nello Pace
Keyword(s):  
Rat Liver ◽  
Equilibrium Concentration ◽  
Liver Mitochondria ◽  
Sodium Ion ◽  
Rat Liver Mitochondria ◽  
Isolated Rat Liver ◽  
Permeability Characteristics ◽  
Diffusion Curve ◽  
Isolated Rat

The rates of penetration of various solutes into isolated rat liver mitochondria have been studied. Sodium, potassium, and sucrose were observed to enter the mitochondria until an equilibrium concentration was reached. The diffusion of these solutes, after the first few minutes, followed the predicted diffusion curve for solutes entering a particle with a rate-limiting membrane and instantaneous mixing in the interior. Reasons for deviations from the predicted equation during the first few minutes of diffusion are suggested. The data show that at pH 7.4 sodium and potassium enter more rapidly than sucrose. I131-labelled albumin was found to enter very slowly, if at all. Increasing the pH from 7.4 reduced the rate at which sodium ion penetrated the mitochondria. The rate of diffusion of sucrose into mitochondria was considerably slower than diffusion of sucrose into a sphere of water of the same size. Sodium ion was not found to be concentrated in vitro against an external concentration gradient as has been reported by other investigators. It is concluded that the rate of diffusion of solutes between the external medium and the interior of mitochondria is probably restricted and controlled by a mitochondrial membrane exhibiting passive permeability characteristics.

scholarly journals Calcium ion cycling in rat liver mitochondria

1978 ◽  
Vol 174 (2) ◽  
pp. 613-620 ◽  
Author(s):  
Chidambaram Ramachandran ◽  
Fyfe L. Bygrave
Keyword(s):  
Rat Liver ◽  
Calcium Ion ◽  
Mitochondrial Membrane ◽  
Initial Rate ◽  
Liver Mitochondria ◽  
Ruthenium Red ◽  
Rat Liver Mitochondria ◽  
Inner Mitochondrial Membrane ◽  
Subsequent Addition ◽  
Unique Mechanism

1. Addition of N-ethylmaleimide to rat liver mitochondria respiring with succinate as substrate decreases both the initial rate of Ca2+ transport and the ability of mitochondria to retain Ca2+. As a result, Ca2+ begins to leave the mitochondria soon after it has entered. Half-maximal effects occur at an N-ethylmaleimide concentration of about 100nmol/mg of protein. 2. The efflux of Ca2+ induced by N-ethylmaleimide is not prevented by Mg2+ or by Ruthenium Red at concentrations known to prevent Ca2+ efflux when exogenous phosphate also is present. Swelling of mitochondria does not accompany N-ethylmaleimide-induced Ca2+ efflux. 3. Addition of Ca2+ to rat liver mitochondria in the presence of N-ethylmaleimide produces an immediate decrease in ΔE (membrane potential), which decreases further to only a slight extent over the next 8min. Concomitant with this is an immediate increase and then levelling off of the −59ΔpH (transmembrane pH gradient). 4. Preincubation of rat liver mitochondria with p-chloromercuribenzenesulphonate, which by contrast with N-ethylmaleimide is unable to penetrate the inner mitochondrial membrane, also prevents Ca2+ retention. The ΔE and −59ΔpH respond to Ca2+ addition in a manner similar to that which occurs when N-ethylmaleimide is present. Subsequent addition of mercaptoethanol produces an immediate increase in both ΔE and −59ΔpH. At the same time Ca2+ is rapidly accumulated by the organelles. 5. The above data are interpreted as indicating that under the conditions of Ca2+ efflux seen here, the mitochondria retain their functional integrity. This contrasts with the uncoupling effect of Ca2+ seen in the presence of Pi, which generally leads to a loss of mitochondrial integrity. We suggest that a unique mechanism of Ca2+ cycling is able to take place when mitochondria have been treated with N-ethylmaleimide.

Effects of 5-5'-Diphenyl-2-thiohydantoin (DPTH) and Thyroxine on the Ultrastructure and Chemical Composition of Rat Liver

1971 ◽  
Vol 29 ◽  
pp. 570-571
Author(s):  
E. A. Elfont ◽  
R. B. Tobin ◽  
D. G. Colton ◽  
M. A. Mehlman
Keyword(s):  
Chemical Composition ◽  
Rat Liver ◽  
Future Study ◽  
Mode Of Action ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Effective Inhibitor ◽  
Biochemical Effects ◽  
Glycerophosphate Dehydrogenase ◽  
Stimulation Of

Summary5,-5'-diphenyl-2-thiohydantoin (DPTH) is an effective inhibitor of thyroxine (T4) stimulation of α-glycerophosphate dehydrogenase in rat liver mitochondria. Because this finding indicated a possible tool for future study of the mode of action of thyroxine, the ultrastructural and biochemical effects of DPTH and/or thyroxine on rat liver mere investigated.Rats were fed either standard or DPTH (0.06%) diet for 30 days before T4 (250 ug/kg/day) was injected. Injection of T4 occurred daily for 10 days prior to sacrifice. After removal of the liver and kidneys, part of the tissue was frozen at -50°C for later biocheailcal analyses, while the rest was prefixed in buffered 3.5X glutaraldehyde (390 mOs) and post-fixed in buffered 1Z OsO4 (376 mOs). Tissues were embedded in Araldlte 502 and the sections examined in a Zeiss EM 9S.Hepatocytes from hyperthyroid rats (Fig. 2) demonstrated enlarged and more numerous mitochondria than those of controls (Fig. 1). Glycogen was almost totally absent from the cytoplasm of the T4-treated rats.

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