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V A Selivanov

Publications and source records attributed to V A Selivanov.

At least 19 recordsLinked to original sources
PubMed2000

Acceptor substrate inhibits transketolase competitively with respect to donor substrate.

Two substrates of the transketolase reaction are known to bind with the enzyme according to a ping-pong mechanism [1]. It is shown in this work that high concentrations of ribose-5-phosphate (acceptor substrate) compete with xylulose-5-phosphate (donor substrate), suppressing the transketolase activity (Ki = 3.8 mM). However, interacting with the donor-substrate binding site on the protein molecule, the acceptor substrate, unlike the donor substrate, does not cause any change in the active site of the enzyme. The data are interesting in terms of studying the regulatory mechanism of the transketolase activity and the structure of the enzyme-substrate complex.

Catalytic Domain↗
PubMed1998

A model of mitochondrial Ca(2+)-induced Ca2+ release simulating the Ca2+ oscillations and spikes generated by mitochondria.

Recent evidence underlines a key role of mitochondrial Ca2+ fluxes in cell Ca2+ signalling. We present here a kinetic model simulating the Ca2+ fluxes generated by mitochondria during mitochondrial Ca(2+)-induced Ca2+ release (mCICR) resulting from the operation of the permeability transition pore (PTP). Our model connects the Ca2+ fluxes through the ruthenium redsensitive Ca2+ uniporter, the respiration-dependent and passive H+ fluxes, the rate of oxygen consumption, the movements of weak acids across the mitochondrial membrane, the electrical transmembrane potential (delta psi), and operation of the PTP. We find that two factors are crucial to account for the various mCICR profiles that can be observed experimentally: (i) the dependence of PTP opening and closure on matrix pH (pHi), and (ii) the relative inhibition of the respiratory rate consecutive to PTP opening. The resulting model can simulate irreversible Ca2+ efflux from mitochondria, as well as the genesis of damped or sustained Ca2+ oscillations, and of single Ca2+ spikes. The model also simulates the main features of mCICR, i.e. the threshold-dependence of mCICR triggering, and the all-or-nothing nature of mCICR operation. Our model should appear useful to further mathematically address the consequences of mCICR on the spatiotemporal organisation of Ca2+ signals, as a 'plug-in' module for the existing models of cell Ca2+ signalling.

Calcium↗
PubMed1998

Kinetic investigation of cooperativity in coenzyme binding by transketolase active sites.

The two-step mechanism of coenzyme (thiamine diphosphate, ThDP) binding with two initially identical active sites of apotransketolase has been examined with a kinetic model. Cooperativity between sites in the primary ThDP binding and in the following conformational transition has been analyzed. The only reliable difference between sites is shown to be the tenfold difference in the backward rate constants of the conformational transition; this means that the cooperative interaction between sites takes place only after termination of both steps of ThDP binding in both sites.

Apoenzymes↗
PubMed1997

Kinetic mechanism of active site non-equivalence in transketolase.

The two-step mechanism of coenzyme (TDP) binding to apotransketolase has been examined by kinetic modeling, and the rate and equilibrium constants for each binding step for two active sites have been determined. The dissociation constants for the primary fast binding step and the forward rate constants for the secondary slow binding step have been shown to be similar for two active sites. The backward rate constants for the secondary binding step are different for two active sites, providing the kinetic mechanism of their non-equivalence in TDP binding.

Binding Sites↗
PubMed1997

Determination of constants of substrate primary binding with baker's yeast transketolase by kinetic modelling.

A kinetic model of bisubstrate reaction catalyzed by baker's yeast transketolase is proposed. The model considers individual stages of substrates reversible primary binding. The model corresponds to the observed kinetics of product accumulation within a wide range of initial substrate concentrations. Kinetic parameters for the best simulation of the experimental data are defined. The equilibrium constants of the primary binding of both the initial and produced ketose and also the initial aldose were unequivocally determined by varying the initial substrate concentrations. The dissociation constants of the primary enzyme-substrate complex for the initial ketose (xylulose 5-phosphate) and the reaction product (sedoheptulose 7-phosphate) were found to differ by more than by two orders of magnitude. The result is discussed in the context of the hypothesis of flip-flop functioning of the transketolase active sites.

Binding Sites↗
PubMed1994

Activity oscillations predicted for pyruvate dehydrogenase complexes.

A kinetic model for the pyruvate dehydrogenase complex is analyzed. The model takes into account intermediate channeling through the lipoyl network attached to the complex core, as well as inter-related regulatory effects of protein X acetylation and enzyme phosphorylation. The model predicts undamped oscillations of enzyme activity.

Kinetics↗
PubMed1990

Graph-theoretic approach to metabolic pathways.

A graph-theoretic approach is shown to be applicable within the framework of the metabolic control analysis. Kinetic differential equations linearized near a steady state are presented as kinetic graphs (schemes), their structure being correlated with kinetic properties of corresponding metabolic networks. The global properties may be expressed in terms of the local properties for steady states of metabolic systems. Instability, bistability, and concentrational oscillations are shown to be induced by specific graph fragments. The approach is illustrated by an example of systems showing the oscillatory kinetic behaviour.

Biotransformation↗
PubMed1985

[Capacity of bone marrow cells to restore thrombocytopoiesis in lethally irradiated animals].

A study was made of the kinetics of thrombocytopoiesis restoration in lethally irradiated mice after transplantation to them of the donor marrow cells. In the initial period, the thrombocytopoiesis restoration is provided by transite cells-precursors of megakaryocytes present in the transplanted bone marrow; the subsequent restoration is due to cells of the self-maintaining population. The level of restoration does not correlate with the number of polypotent cells that form macrocolonies in the spleen of irradiated recipients.

Animals↗
PubMed1984

[Comparison of 2 methods of studying polypotent hematopoietic cells].

The cells giving rise to colonies in the spleen of a lethally irradiated recipient after their transplantation (exogenous CFUs) have a higher self-maintaining ability than those that repopulate their own hemopoietic territory after irradiation, due to the migration of these cells from screened territories (endogenous CFUs). The number of exogenous CFUs and their self-maintaining ability do not change with animals ageing.

Aging↗
PubMed1984

[Patterns of thrombocytopoiesis regulation].

Based on literature data, the main kinds of thrombocytopoiesis regulation are analyzed. It is shown that humoral factors regulate the intensity of proliferation of committed precursors and the mean sizes of mature megakaryocytes. The activity of these factors depends on the numbers of thrombocytes in blood and of megakaryocytes in bone marrow. The evidence presented in the review enables one to give a quantitative description of the relationship between the rate of thrombocytopoiesis and the content of thrombocytes in blood. The fact that the alteration of the time of megakaryocyte maturation does not depend on the duration and strength of the influences points to a non-specificity of this reaction. A scheme for the thrombopoiesis regulation is proposed which can serve as a basis for its mathematic description.

Blood Platelets↗
PubMed1984

[Regulation of thrombocytopoiesis studied by a mathematical model].

A mathematical model of thrombocytopoiesis is proposed which accounts for the recent data on its regulation. It is shown that the compensatory response of the system to a decrease in the level of thrombocytes in the blood is controlled by the total amount of thrombocytes and megakaryocytes. The proliferation intensity of megakaryocytes and the total number of thrombocytes reveal, respectively, a lineary and a logarithmical dependence on the total number of thrombocytes and megakaryocytes. The limits of the post-transfusion level of thrombocytes are defined, within which the thrombocytopoiesis is controlled only by the number of thrombocytes. The values of parameters characterizing the behaviour of the thrombocytopoiesis system are calculated.

Animals↗
PubMedDate not supplied

[Elaboration and introduction of an algorithm of rendering the anesthetic-and-resuscitation care to a big number of wounded person in terrorist attacks].

Medical records of 320 persons, who were injured in terrorist attacks in 1999-2003, were analyzed. The main errors in rendering the anesthetic-and-resuscitation care were pointed out. An algorithm of actions is elaborated for the anesthesiologist working at the reception, surgical and intensive care departments of a hospital. Owing to the mentioned algorithm, the lethality rate of wounded persons dropped from 18 to 10%.

Algorithms↗
PubMedDate not supplied

[A study of the effect of radiation on megakaryocytopoiesis using a mathematical model].

Mathematical modelling used in analysing the postirradiation changes in megakaryocytopoiesis permitted to determine the level of radiation-induced injury in each experiment conducted and to show that megakaryocytopoiesis regulation followed the same mechanism after irradiation as it does normally and after the effect of hydroxyurea and anti-thrombocyte serum. The analysis has demonstrated that after the stem cell death induced by ionizing radiation, the regeneration can be provided by the committed cells, and the level of regeneration is determined by the maturity of precursors.

Animals↗