[Binding of lipopolysaccharide and complexes of lipopolysaccharide with serum low density lipoproteins to liver macrophages].

Binding of [3H]-lipopolysaccharide toxin (LPS) and complexes of LPS with serum [125I]-labeled low density lipoproteins (LDL) with primary culture of rat liver macrophages (Kupffer cells) has been studied. Total, specific and nonspecific binding was determined. The receptor interaction was shown to dominate for both LPS and LDL-LPS complexes, amounting to 70-77% and 80-85%, respectively.

[Properties of Na+/HCO3-(Cl-)-stimulated ATPase in rabbit small intestinal mucosa].

It has been demonstrated that histamine induces in rabbit small intestine an ATPase activity which is stimulated by NaCl or NaHCO3. The Na+/HCO3- (C1-)-stimulated ATPase activity, unlike the Mg2+,HCO3(-)-ATPase activity, has a pH optimum at pH 6.2, is inhibited by ethacrynic acid (10(-4) M) and bivalent metal ions (but not 10(-2) M thiocyanate).

[Features of regulatory system function in platelets under the effect of plague toxin].

Yersinia pestis toxin (II fraction by E. Baker) inhibited aggregation of human platelets as well as elevation of Ca2+, induced by different agonists ADP, PAF, thrombin. Agonist-induced Ca2+ mobilization and Ca2+ influx were dose-dependently inhibited by the toxin.

[Hormonal regulation of carbohydrate metabolism in the liver in plague intoxication].

It was shown that "mouse" toxin of Yersinia pestis injected into the rat tail vein (LD100) caused a 2-fold decrease in the glycogen content in the liver and the glucose content in the blood. The Bmax of beta-adrenoceptors as well as basal, forskolin, 5-guanylyl imidodiphosphate, fluoride and glucagon-stimulated liver adenylate cyclase (AC) activities did not change in all periods of intoxication. After 5 hours of intoxication isoproterenol had no effect on AC; however, the cAMP content was increased 1.

[The capacity of Yersinia pestis toxin to decrease the functional response of human thrombocytes to stimulation by hormones].

Yersinia pestis toxin (fraction II by E. Baker) (YPT) inhibited the aggregation of human platelets as well as elevation of [Ca2+], induced by different agonists (ADP, PAF, Thrombin). Agonist-induced Ca2+ mobilization and Ca2+ influx were dose-dependently inhibited by the toxin.

[The mechanism of the inhibiting effect of a Yersinia pestis protein factor on the hormone-stimulated response of human thrombocytes].

Thermostable protein factor (20000 Da) was prepared from Yersinia pestis avirulent strain EV 1290. This protein inhibited the aggregation of human platelets as well as elevation of [Ca2+], induced by different agonist. The action of this protein on platelets is accompanied by elevation of cellular cGMP levels.

[Regulatory properties of the rat heart adenylate cyclase in the course of toxic-infective shock caused by Yersinia pestis].

Influence of intravenously administered to rats murine toxin of Y. pestis in the dose of I mg/ml (LD100) on the regulatory properties of heart plasma membranes adenylate cyclase (AC) has been studied during the intoxication. It has been shown that basal, fluoride,- and 5-guanylyl imidodiphosphate-stimulated AC activity remained unchanged during the intoxication.

[Potential-dependent Ca2+ channels and contractile function of the heart in toxic-infectious shock caused plague].

Influence of intravenous administration to rats of murine toxin of Y. pestis (1 mg/ml, LD100) on the number of potential-operated Ca(2+)-channels, alpha- and beta-adrenergic and M1-cholinergic receptors of plasma membranes and heart contractility function has been studied in rats. The number of Ca(2+)-channels in plasma membranes and contractility of heart decreased by 50% in 1 hour after the i.

[Glutathione and superoxide dismutase redox system in the development of toxic-infectious shock caused by Yersinia pestis toxin].

The changes in the glutathione-dependent and superoxide dismutase (SOD) enzymatic activity in the rat lungs and liver tissues have been studied after the administration of plague murine toxin (LD100). It has been found out the early toxic effect in 1h in the lungs: 35% SOD and glutathione peroxidase (tributyl hydroperoxide) (GP) decrease, 87% glutathione reductase (GR) increase along with two-hold ascent of ratio GR/Glutathione-S-transferase (GT), GR/GPs. The fundamental ratio GR/GT.

[The enzymatic antioxidant system of the thrombocytes in meningococcal infection].

A study was made of the time-course of changes in the activity of the enzymic antioxidant system of blood platelets from patients with meningococcemia and meningitis (mixed form) of medium gravity. As a result a steady unbalance in the redox system of glutathione was established: a decrease of glutathione reductase activity and rise of the activity of glutathione peroxidases to hydrogen peroxide and tertiary butyl hydroperoxide until the clinical recovery. The patients with meningococcal meningitis and with the mixed form of medium gravity manifested impairment of the interrelations between superoxide dismutase and glutathione peroxidase to hydrogen peroxide, with that impairment being eliminated by the end of the disease.

[The functional characteristics of the enzymatic antioxidant system in the erythrocytes and neutrophils of the blood of patients with generalized forms of meningococcal infection].

Patients with meningococcal infection, meningitis and with a mixed form of the disease were demonstrated to have unbalance in the redox system of glutathione during the all disease periods till the clinical recovery. Activation of glutathione peroxidases to hydrogen peroxide and tertiary butyl hydroperoxide in erythrocytes was coupled, during the whole disease, with unbalance of the time-course of changes in the interrelated enzymes--superoxide dismutase and glutathione peroxidase to hydrogen peroxide, while in neutrophils, the balance of those enzymes remained unimpaired. Glutathione transferase activity appeared reduced both in erythrocytes and neutrophils.

[Structure of the lipopolysaccharide/human plasma low density lipoprotein complex. 31P-NMR and fluorescence spectroscopy studies].

Complexes of Salmonella typhimurium lipopolysaccharide toxin (LPS) with low density lipoproteins (LDL) containing various amounts of LPS were prepared in vitro. The 31P-NMR spectra showed that in the LDL-LPS complexes as well as in native LDL all phosphate groups of phospholipids are accessible to the paramagnetic shift reagent, Pr3+. Besides, the low frequency mobility of phospholipid phosphates in the complex is diminished.

[Effect of lipopolysaccharide toxin on lipid and protein composition of human serum low density lipoproteins].

Complexes of lipopolysaccharide (LPS) B of Salmonella typhimurium with human low density lipoproteins (LDL) formed during in vitro coincubation via spontaneous incorporation of LPS (complex LDL-LPS) or through the incorporation stimulated by the serum protein fraction (LPS/LDL complex) were studied. The LPS/LDL complex was shown to maximally bind 0.24 mg of LPS per 1 mg of LDL protein, whereas the LDL-LPS complex contained only 0.

[Effect of the lethal Bacillus anthracis toxin on phagocytosis and the dynamics of the change in the enzyme activity of the antioxidative system of peritoneal mononuclear phagocytes in mice with differing hereditary immunity to anthrax].

It was demonstrated, that the lethal in vitro suppressed the phagocytic activity of peritoneal mononuclear phagocyte (Mph) and enhanced the level activity of glutathione peroxidase to H2O2 (GP-H2O2) in Mph of resistant to anthrax BALB mice. In Mph BALB the authors observed dependent-dose enhancement of GP-H2O2 activity and reduction of the ratio of level glutathione reductase (GR) to GP-H2O2 (GR/GP-H2O2). The enhancement of activity GR-H2O2 in Mph CBA was not dependent on the doses of toxin.

[Effects of Y. pestis mouse toxin on carbohydrate metabolism in rats].

Effects of intravenous Y. pestis mouse toxin (LD50) injection on glucose, lactate glucagon, insulin blood levels and cAMP liver content in dynamics of intoxication development were studied. Hypoglycemia, observed 2 hours after toxin administration seems not to be due to the enhanced glucose utilization in peripheral tissues because insulin blood level during this period was decreased and lactate concentration has not been changed.

[Low molecular weight and protein dinitrosyl complexes of non-heme iron as inhibitors of platelet aggregation].

Dinitrosyl complexes of ferrum with thiosulfate or reduced glutathione were found to inhibit completely aggregation of human thrombocytes, suspended in artificial protein-free medium. The inhibitory effect appears to occur as a result of activating action of nitrogen oxide derived from the complexes and affecting the thrombocyte guanylate cyclase.

[Lipopolysaccharide-induced hydrolysis of plasmalogenic phosphatidylethanolamine in human platelets].

The composition of human platelet major phospholipids-phosphatidylcholine (PC), phosphatidylinositol (PI), phosphatidylserine (PS), phosphatidic acid (PA), sphingomyelin (SM), plasmalogenic and diacyl species of phosphatidylethanolamine (PPE and APE, respectively) was quantitatively analyzed by high performance liquid chromatography. Incubation (10 min, 37 degrees C) of washed platelets with lipopolysaccharide B (LPS) of Salmonella typhimurium was found to produce (in the absence of aggregation) marked hydrolysis of PI (ca. 15%) and PPE (ca.

[Levels of prostaglandin E1 and F2 alpha in the dynamics of toxic-infectious shock induced by Yersinia pestis].

Murine toxin of Yersinia pestis when injected in the rat tail vein (LD50) caused pronounced alterations in PGE1 and PGF2 alpha content in different tissues (lung, heart, spleen, liver, kidney, small intestine) and blood. Heat-inactivated toxin has been shown to have the same effects as the intact toxin preparation. The changes in PG content are, probably, due to the lipopolysaccharide component of both preparations.