Publications by authors named "Kharlamova O"

In experiments in vivo we studied the interaction between two ion-transporting mechanisms of cardiovascular system--Na+, K+ -ATPase of rat aorta and Ca2+ -uptake system of mitochondria in short-term response to different doses of NO donor, nitroglycerine (NG). The activity of the Na+, K+ -ATPase was determined in rat aorta, and mitochondrial uptake of Ca2+ was studied in rat heart mitochondria assuming that metabolism induced by NO in cardiac mitochondria is similar to that in rat aortic mitochondria. The data show a coordinated dose-dependent action of NG on Na+, K+ -ATPase activity as well as Ca2+ -uptake in mitochondria.

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The influence ofnitric oxide on Na+,K(+)-ATPase activity in rat aorta was studied by means of stimulation of endogenous NO synthesis after injections of bacterial lipopolysaccharide (LPS) and pharmacological NO donor nitroglycerine (NG). It was shown that NO action on Na+,K(+)-ATPase in vivo is dose-dependent. Stimulation of the endogenous NO synthesis by LPS as well as the administration of low doses of NG lead to the activation of Na+,K(+)-ATPase and favor the conclusion that NO-dependent Na+,K(+)-ATPase stimulation mediates vasodilatory and hypotensive action of nitric oxide.

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Aluminum chloride was tested for its effect on primary T-dependent humoral immune response. The administration of aluminum chloride in the genotoxic dose (0.04 M) caused in mice a profound immunosuppressive effect accompanied by diminished thymic and splenic cellularity.

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Views of the toxicity of aluminum to man, animals, and plants and on its behavior in the ecosystems with a changing man-made loading have changed in the past 30 years. Aluminum along with its human medical consequences has been found to present problems on the acid soils in world agriculture. To systematize knowledge and to control information on aluminum and its compounds, the reference information system "Ecology and Aluminum Toxicology" whose structure is based on the developed model of an ecological aluminum cycle was designed.

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The influence of NO donor, sodium nitroprusside (SNP) in concentrations of 10(-5)-10(-3) M, on the Na-pump activity in membrane preparations (microsomes) of rat miocardium and renal cortex was studied. A correlation has been observed between Na-pump activation by 31.4% and 73.

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Ascorbic acid has wide usage in medical practice for treatment some diseases caused by degeneration of connective tissue. Ascorbic acid has strong reduce properties. This article is dedicated to investigating complexation properties of ascorbic acid with components of biomembrans-bioligands: the most widespread aminoacids of connective tissue, phosphatidylholine, ATP, calcium salts, proteins.

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The effect of L-arginine on the Na+,K+-ATPase activity in rat aorta endothelium was studied at its physiological concentrations in the range of 10(-6)-10(-3) M. The enzyme activity was 35.5% increased by low concentrations of L-arginine ( View Article and Find Full Text PDF

In the combination of gel- and ion exchange chromatography low-molecular weight (Mm < 1000 Da) fractions of tissue extracts of small intestine epithelium with high activity towards the Na+,K(+)-ATP-ase were obtained. The influence of these fractions on the Na+, K(+)-ATP-ase of small intestine epithelium and rat renal cortex is studied and discussed.

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The study was undertaken to elucidate the effects of taurine on lipid peroxidation (LP) intensity and membrane Na+, K+-ATPase activity in a hypoxic rat model. It was shown that 3 intraperitoneal (i.p.

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The influence of precursor of biosynthesis of nitric oxide L-arginine on the level of transport enzymes Na+, K(+)-, Ca(2+)- and Na(+)-ATPases activity under rabbits experimental hypercholesterolemia have been studied. The significant changes in Na+, K(+)-, Ca(2+)- and Na(+)-ATPases activity in different tissues (the cortex of kidney, the endothelium of aorta, the epithelium of small intestine, the liver) had been found for the rabbits with inhibition of the activity of this enzymes to the different levels in all these tissues. Injection of L-arginine during the hypercholesterolemia caused the recovery of Na+, K(+)-, Ca(2+)- and Na(+)-ATPases approximately to the control levels.

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It was found that preliminary treatment by amino acid taurine protected rats from lipid peroxidation intensification (expressed in terms of malondialdehyde and conjugated dienes contents) in the liver, brain and heart under acute severe normobaric hypoxic hypoxia. The mechanisms of the antioxidant action of taurine are connected to the prevention of lactate accumulation in tissues and cell membrane structure disorders (expressed in a decrease of membrane Na+, K(+)-ATPase activity). It was also shown that taurine reduced significantly a decrease of glutathione antioxidant system activity protecting tissues against reduced glutathione pool depletion and preventing a decrease of glutathione reductase and glutathione peroxidase activities in acute severe hypoxia.

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From epithelial layer of rat intestinal were selected water soluble substances which influenced on Na+,K(+)-ATPase activity in 2 different ways: substances with molecular weight 220 Da, 400 Da were its activators, substance with weight 150 Da-inhibitor. Na+,K(+)-ATPase activators preincubated previously with Na+ acquire properties of inhibitors. Bivalent cations Ca, Mg remove this effect of Na-ions.

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The activities of Na+, K(+)-ATPase and 5'-nucleotidase of the plasma membranes, Ca++, Mg(++)-ATPase of the sarcoplasmic reticulum, mitochondrial cytochrome C-oxidase and succinate dehydrogenase were investigated in the brain, liver and gastrocnemius muscle of Wistar rats at various terms of adaptation to hypoxic hypobaric intermittent hypoxia. An increase in the activity of Na+, K(+)-ATPase and mitochondrial enzymes (mostly in the liver) as well as in the activity of Ca++, Mg(++)-ATPase in the skeletal muscle beginning from 14 days of adaptation have been shown. Starting with the same term the authors have registered the less marked changes of the enzymic markers of cell membranes in adapted rats under additional acute and severe hypoxic test when compared to unadapted animals.

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Activity of transport Na+, K(+)-ATP-ase has been studied both in the ischemia-affected proximal section of the small intestine and in tissues which did not endure ischemia (the brain, renal cortex and the distal part of the small intestine) in dynamics 5, 30 and 60 min, after reperfusion of the ischemized small intestine of rats. It is shown that after 30 min-long ischemia of the small intestine, the Na+, K(+)-ATP-ase activity is inhibited in all the tissues mentioned. Maximal inhibition of the enzyme activity after 30 min long reperfusion is 74, 34, 94 and 58% for the brain, renal cortex, proximal and distal sections of the small intestine, respectively.

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Experiments on Wistar rats injected intragastrically deionized water (1 % of the body weight) and intra-abdominally 0.1 mg/kg of the lyophilized water extract (LWE) from the thin intestine have shown that under these conditions diuresis and excretion of K+ with the urine increase and retention of Na+ excretion decreases. After intragastric injection of isotonic NaCl solution, the LWE has exerted only the K-excretion effect.

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The membrane activity of Na+, K(+)-ATPase, Mg2+, Ca(2+)-ATPase, mitochondrial NAD-isocitrate dehydrogenase, mitochondrial and cytosolic L-glycerol-3-phosphate dehydrogenase was determined in the liver and brain of Wistar rats under acute hypoxic hypoxia against the background of preventive taurine administration. It was shown that preliminary taurine treatment prevented a decrease of hypoxia in activity of Na+. K(+)-ATPase and mitochondrial calcium-dependent enzymes, mostly in the liver.

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The experiments on Wistar rats have shown that intragestral injection with mannitol hypotonic solution (20 mmol/l) causes the significant activation of Na+, K(+)-ATPase of duodenum and distal intestine epithelial cells, kidney cortex cells, but does not affect the brain cortex of Na+, K(+)-ATPase activity. Simultaneously the activator of enzyme (AE) enters blood serum of rats, its activity is revealed by blood serum addition to homogenates of tissues of control rats. It is assumed that AE is produced in duodenal and intestinal mucosa released to blood after stimulation of mucosal surface by hypotonic solutions and included into the osmoregulation processes on the Na+, K(+)-ATPase level.

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The experiments in vitro have shown that perfusion of the isolated duodenum cavity in rats by hypotonic (20 mosmol/l H2O) or hypertonic (500 mosmol/l H2O) solutions of NaCl and mannitol during 10 min stimulates secretion of endogenic factors (activators or inhibitors of enterocytes of Na+, K(+)-ATPase) into the serous incubation solution. Contact of the duodenum mucose surface with isotonic (300 mosmol/l H2O) solutions does not stimulate the secretion of this enzyme regulators. Endogenic substance are thermostable: they retain activity relative to Na+, K+ ATPase of enterocytes after heating (100 degrees C, 10 min duration) of serous incubation solutions.

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Intragastric administration of mannitol or NaCl hypotonic solution induced a significant shift of the electrolyte balance in the small intestine epithelium, and activated the enterocytes' Na,K pump in Wistar rats. De-ionised water caused the maximal enhancement of the Na,K-ATPase activity, whereas hypertonic solutions exerted the opposite effect, a substance-inhibitor appearing in the blood serum. Similar results were obtained in vitro.

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Experiments on rats have shown that intragastric single introduction of mineral water Naftusia to animals in a dose of 1.5% of the body weight of animals induces sodium accumulation in the small intestine epithelium, that is a result of Na(+)-, K(+)-pump inhibition by fatty acids of this water. Naftusia absorption induces appearance of inhibitors of Na(+)-, K(+)-ATPase enzymic system in blood serum of rats.

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