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V P Zinchenko

Publications and source records attributed to V P Zinchenko.

At least 55 records · Page 3Linked to original sources
PubMed1982

Induction of 2H+/Me2+ exchange in rat-liver mitochondria.

The time dependency of CA2+ efflux from Ca2+-loaded rat liver mitochondria has been investigated. The rate of ruthenium-red-insensitive Ca2+ efflux is continuously increased during the retention as a result of induction of an electroneutral H+ Ca2+ exchange system. The activation of the Ca2+ efflux pathway takes place under the constant value of the membrane potential and is accompanied by oxidation of mitochondrial pyridine nucleotides. It has also been found that the ruthenium-red-insensitive H+/Sr2+ exchange occurs in mitochondria during Sr2+-induced oscillation of ion fluxes. The rate of H+/Sr2+ exchange is variable and depends on the stage of the oscillatory cycle.

Animals↗
PubMed1982

[Reversible changes in the volume of isolated mitochondria in the course of ion flux oscillations between the mitochondria and the medium].

Glutaraldehyde has been used for electron microscopic studies of mitochondrial volume fluctuation during Sr2+--induced oscillation of ion fluxes. It has been shown that the observed ultrastructural and fluctuations of mitochondria is reversible to correlate with light-scattering value as well as to the direction of ion transfer. Determination of the intramitochondrial volume at different stages of oscillatory cycle shows the increase in the volume during the process of swelling up to 2.4-5.6 times compared with the shrihkate state.

Animals↗
PubMed1982

[Description of mitochondrial K+-transport system during intensive physical work].

The content of potassium ions in rat liver mitochondria after intensive physical work (continuous swimming) is increased approximately 2-fold, while the rate of K+ efflux from the mitochondria is significantly reduced. A considerable increase of the "calcium capacity" and a decrease of the respiration rate in state 4 were found. The experimental results indicate that during intensive physical work the mitochondrial membrane resistance to the damaging effects is enhanced. A possible mechanism of these changes is discussed.

Animals↗
PubMed1982

[Kinetics of oxygen consumption, luminescence of pyridine nucleotides and the cyanine dye 3',3'-diethylthiodicarbocyanine iodide after energizing Ehrlich ascites carcinoma cells with glucose].

It has been shown that in the absence of inhibitors of oxidative phosphorylation, changes in fluorescence of 3',3'-diethylthiodicarbocyanine iodide (dis-C2-/5/) in a cell suspension of Ehrlich's ascites carcinoma reflect those in the transmembrane mitochondrial potential. Addition of glucose to the cells in the presence of respiratory inhibitors similar to rotenon induces oscillations in the membrane mitochondrial potential due to H+-ATPase that uses glycolytic ATP. The described changes in energy metabolism parameters are determined by impairment of the interplay between glycolysis and oxidative phosphorylation. The low rate of cytoplasmic NADH oxidation by tumor cell mitochondria favors the latter's accumulation by the cytoplasm and glycolysis inhibition. Pyruvate has been shown to be responsible for NADH oxidation and to remove glycolysis inhibition.

Animals↗
PubMed1981

[State of cardiac pyridine nucleotides and flavoproteins during preservation with a 0.5% formalin solution].

Possibilities of formaldehyde interaction with the respiratory link of mitochondria were studied. For this purpose the fluorescent technique was used to examine pyridine nucleotides and flavoproteins of the conserved heart. The data obtained indicate that the action of formaldehyde on oxidation myocardial cell metabolism appears to be related to the inhibition of the glycolytic apparatus.

Animals↗
PubMed1980

The stoichiometry of ion fluxes during Sr2+-induced oscillations in mitochondria.

A quantitative study of H+, K+, Sr2+ and succinate fluxes in Sr2+-induced oscillatory state of rat liver mitochondria is presented. It was shown that oscillation of succinate content in mitochondria occurs synchronously with oscillations of the cation fluxes. Total charge transferred across the membrane by the registered cations and the succinate-anion is equal to zero. Passive H+-influx has been calculated at all stages of the oscillatory cycle. The conclusion is made that electroneutral 2 H+/Sr2+ exchange is periodically induced in mitochondria. A value of (2 +/- 0.2) . 10(-7) mol Sr2+/min per mg protein has been determined for Sr2+ by this type of exchange.

Animals↗
PubMed1977

[Ca2+ ion transport in the mitochondria of Ehrlich ascites tumor cells].

Peculiarities of Ca2+ accumulation in tumor mitochondria (TM) under different experimental conditions were studied. In the absence of penetrating anions TM were shown to accumulate Ca2+ five times less than liver mitochondria do, this difference being even more in the presence of acetate. pi abolishes the observed defects in Ca2+ transport while increasing considerably the Ca2+-capacity of TM. Besides, as distinct from liver mitochondria, Pi produces a stabilizing effect upon the membrane permeability of TM, which can be responsible for the increase in the TM Ca2+-capacity.

Absorption↗
PubMedDate not supplied

[The role of intracellular Ca(2+) pools in the regulation of protoplast volume. Effect of red light on the Ca(2+) mobilization in cytoplasm of Arabidopsis cells].

The changes in cytosol Ca2+ concentration associated with the shrinkage of Arabidopsis cells induced by the inhibitor of Ca(2+)-ATPase, cyclopiazonic acid and the Ca2+ ionophore ionomycin were monitored using the fluorescence of Ca(2+)-sensitive probe chlortetracycline hydrochloride. It was found that these compounds elicited a substantial decrease in fluorescence intensity closely associated with Ca(2+)-release from the intracellular stores to the cytoplasm. The release of Ca2+ from the intracellular depots was accompanied by decrease of plant cell volume. Thapsigargin and 2,5'-ditert-butyl-1,4-benzohydroquinone (highly specific inhibitors of Ca(2+)-ATPase of endoplasmic reticulum) resulted in much weaker changes than cyclopiazonic acid did. It was also found with the help of the same technique that red light (lambda = 660 nm) illumination induced a similar Ca2+ release from the intracellular stores. Moreover, the amplitudes of light-induced fluorescence responses registered in mutant plants differing in the content of phytochrome A (phyAOX) and phytochrome B (phyBOX) were much higher than those registered in wild-type of Arabidopsis.

Arabidopsis↗
PubMedDate not supplied

[Analysis of the kinetics of Ca2+ signals in Ehrlich ascites tumor cells upon the inhibition of the mitochondrial Na+/Ca2+ exchanger].

Signals of cytosolic Ca2+ (Ca2+c) and mitochondrial Ca2+ (Ca2+m) evoked by the activation of purinoreceptors of Ehrlich ascites tumor cells at different extents of inhibition of the mitochondrial Na+/Ca2+ exchanger by tetraphenylphosphonium (TPP+) were investigated. [Ca2+c] was measured by Fura-2 fluorescence, and [Ca2+m] changes were inferred from NAD(P)H fluorescence. The addition of ATP to the cell suspension induced a NAD(P)H response, which replicated Ca2+c signal with some retardation of the peak and a slower decay. In the presence of increasing TPP+ concentrations, NAD(P)H responses evidenced that the rate of [Ca2+m] decay strongly decreases, while the phase of initial rise does not change. The maximal TPP+ dose did not affect [Ca2+c] and NAD(P)H fluorescence in the resting state, as well as ATP-induced [Ca2+c] responses. These data are described in a mathematical model, which accounts for Ca2+ transport through the membranes of endoplasmic reticulum and mitochondria, as well as through the plasma membrane. The model indicates a low rate of the mitochondrial cycle of Ca2+ uptake/efflux at rest and a strong activation of the uptake with increasing [Ca2+c] to which a Hill coefficient of no less than 4 corresponds. Furthermore, the rise of the uptake rate changes in a short time to a decline, and the peak of the rate is markedly ahead of the peak of [Ca2+c].

Adenosine Triphosphate↗
PubMedDate not supplied

[The calmodulin inhibitor R24571 induces a short-term Ca2+ entry and a pulse-like secretion of ATP in Ehrlich ascites tumor cells].

The properties of the Ca2+ channel induced by a calmodulin inhibitor in Ehrlich ascites tumor cells were investigated using fluorescent indicators Indo-1 and chlortetracycline. The inhibitor of calmodulin calmidazolium (R24571) in concentrations of 1-2 microM induces a short-term Ca2+ entry and a pulse-like ATP secretion. Repeated addition of R24571 also causes a transient Ca2+ signal. Ca2+ channels induced by R24571 are permeable for Mn2+. Ca2+ entry does not depend on endoplasmic reticulum depletion by thapsigargin, ATP, or ionomycin and is suppressed by nordihydroguaretic acid (EC50 = 6.7 microM), quercetin (EC50 = 1.5 microM), dihydroquercetin (EC50 = 17 microM), arachidonic acid (AA) (EC50 = 8.6 microM), and suramin (EC50 = 0.25 +/- 0.05 MM), and weakly depends on temperature in the range of 18 - 37 degrees C. The apparent activation constant for R24571 and the Hill coefficient are 2.5 +/- 0.2 and 4 +/- 0.3 microM, respectively. The products of arachidonic acid oxidation are neither activators nor inhibitors of these channels. The inhibitory effect of nordihydroguaretic acid is indirect and is conceivably caused by the accumulation of arachidonic acid due to suppression of its lipoxygenase-catalyzed oxidation at phospholipase A2 activation. The maximal level of about 1.3 microM in the dependence of Ca2+ signal amplitude on R24571 concentration points to possible inhibition of the channel by increased Ca2+ concentration in the cytosol. The weak dependence on temperature implies that the channel is highly permeable, the chain of enzymic processes is not involved in Ca2+ entry activation, and the mutual compensation of processes with opposite contributions is possible. Using chlortetracycline fluorescence, we have shown in model experiments on calmodulin solution that Ca2+ induces cooperatively a conformational transition of calmodulin with the exposure of a hydrophobic chlortetracycline-Ca(2+)-binding site. The interaction of R24571 with the CaM-Ca2+ complex results in quenching of fluorescence to its level in water, which is interpreted as the elimination of the availability of calmodulin hydrophobic site for chlortetracycline-Ca+. Nordihydroguaretic acid, quercetin, and dihydroquercetin, but not suramin, also interact with calmodulin, but this does not result in the complete closing of its hydrophobic site. It is supposed that the activation of the Ca2+ channel occurs owing to the activation of calmodulin-dependent phospholipase A2 by R24571, which leads to the formation of a low-molecular short-lived secondary messenger, or because of the interaction of R24571 with calmodulin, which directly inhibits the channel. The termination of Ca2+ entry is probably due to the inhibition of phospholipase A2 and/or of the channel at increased concentrations of arachidonic acid and Ca2+.

Adenosine Triphosphate↗
PubMedDate not supplied

[Changes in pH in the cytoplasm of rat thymocytes after treatment with the mitogen concanavalin A and protein kinase C activator phorbol ester].

The intracellular pH (pHi) of rat thymocytes has been measured with the fluorescent probe 2', 7'-bis(carboxyethyl)-5,6-carboxyfluorescein, both in the resting cells and under mitogenic stimulation. Concanavalin A (Con A) has been found to increase pHi from 7.16 +/- 0.02 to 7.30 +/- 0.02 during the first minutes after addition; the phorbol ester TPA raised pHi to 7.25 +/- 0.02. The Con A- and TPA-induced rise of pHi is due to activation of Na+/H+ exchange since it was abolished by amiloride, an inhibitor of Na+/H+ antiport, or in a low-Na+ medium. The elevation of intracellular cAMP level, decrease of cellular ATP, or the lowering of the temperature from 37 degrees down to 25 degrees C inhibited the pHi rise induced by Con A or TPA.

Animals↗
PubMedDate not supplied

[The effect of spermine on transport of Ca2+ ions in brain mitochondria].

The effect of spermine (50-400 microM) on the Ca-transporting system of brain mitochondria was studied. In a medium containing Mg2+ and ATP, spermine facilitates the accumulation of Ca2+ by decreasing Km of the uniporter. Spermine inhibits Na-stimulated Ca2+ efflux; this effect is dependent on the ionic strength of the medium--it is decreased when KCl concentration is increased from 20 to 120 mM. Spermine (200 microM) decreases (by 50%) the steady state concentration of Ca2+ maintained by mitochondria. The importance of spermine as a regulator of Ca2+-transport in brain mitochondria is discussed.

Animals↗
PubMedDate not supplied

[Effect of Ca ions on the transmembrane electric potential, synthesis and hydrolysis of ATP in brain mitochondria].

The transmembrane potential (delta psi) of rabbit brain mitochondria was measured with the fluorescent dye dis--C2--5. During oxidative phosphorylation a fall in delta psi in the order of 20% was observed. In the presence of inhibitors of ATP synthesis, there was a good correlation between the fall in delta psi and the ADP-stimulated increase in respiration rate. The influence of endogenous calcium on the energetic metabolism of mitochondria was studied by measuring the changes of delta psi. An amount of 12 nmol Ca2+/mg protein cause half-inhibition of the ATP synthesis rate; 50 nmol/mg completely inhibits oxidative phosphorylation. The effect of the Ca2+ load on the ATPase activity of intact mitochondria was studied. It was found that endogenous calcium inhibits in a similar degree synthesis and hydrolysis of ATP. It was shown that both Ca ATP and Mg ATP can serve as a substrate for the mitochondrial ATPase.

Adenosine Triphosphate↗