[Phosphoinositide metabolism in endothelial cells of the human umbilical vein exposed to Y. pestis toxin].
Explore the source record for details and available documents.
Bacterial Toxins↗
Biomedical subjects
T D Cherkasova
Publications and source records attributed to T D Cherkasova.
[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 1.5 times in comparison with control. These data suggest that plague intoxication has no effect on cAMP-dependent regulation of glycogenolysis and gluconeogenesis in the liver. The action mechanism of toxin(s) on carbohydrate metabolism in also unrelated to the decrease in Bmax for alpha 1 adrenergic receptors in liver membranes, whose number increased 1.3 and 1.5 times after 1 and 2 hours of intoxication.
Adenylyl Cyclases↗
[Regulation of the adenylate cyclase system of the rat lungs in Yersinia pestis intoxication].
Explore the source record for details and available documents.
Adenylyl Cyclases↗
[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 effect was rapid, developing during the first minute of incubation with toxin. In contrast to murine lethal protein (MLP), the platelet-inhibiting activity was thermostable and was eliminated in the course of MLA purification from YPT. These data indicate that Yersinia pestis component, unlike MLP, could influence the Ca(2+)-dependent processes in human platelets.
Adenosine Diphosphate↗
[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. Stimulation of AC by isoproterenol, glucagon and histamine did not change during the first two hours and significantly decreased after 5 hours of intoxication. Affinity of AC for the investigated hormones did not change through the experiments.
Adenylyl Cyclases↗
[The prostaglandin and cyclic nucleotide levels in the organs of mice with experimental anthrax intoxication].
In this work the influence of Bacillus anthracis toxin, introduced intraperitoneally in a dose of LD100, on the content of prostaglandins E and F2 alpha, 6-ketoprostaglandin F1 alpha, thromboxane, cAMP and cGMP in the lungs, heart, liver and spleen of BALB/c mice in the time course of experimental intoxication has been studied. The concentration and proportion of prostaglandins and cyclic nucleotides have been shown to undergo-sharp changes in all organs under study in the process of intoxication. The level and proportion of prostaglandins in the lungs ensures the development of vaso- and bronchodilatation processes even at early stages of the action of the toxin. B. anthracis toxin sharply increases the content of cGMP in the organs under study and cAMP in the liver. The activating effect on the adenylate cyclase system of tissue cells is not linked with the action of the edematous factor of the toxin. The role of cyclic nucleotides and prostaglandins in the development of pulmonary edema in intoxication with B. anthracis toxin is discussed.
Animals↗
[Cyclic nucleotides, prostaglandins and thrombocyte aggregation in rats poisoned with "murine" Yersinia pestis toxin].
Y. pestis "mouse" toxin, introduced intraperitoneally into rats in a dose of LD100 [correction of LG100], produces phasic changes in the thrombin-induced aggregation of thrombocytes and the content of prostaglandins and cyclic nucleotides in them. As the result of the damaging action on the endothelium of blood vessels at the initial period of intoxication, the concentration of prostaglandin 6-keto F1 alpha in blood plasma and cAMP [correction of cAMR] in thrombocytes sharply decreases, which causes the enhancement of thrombin-induced cell aggregation. At a later period the level of prostaglandin E in the cells sharply rises. At later irreversible stages of shock, induced in the cells of Y. pestis "mouse" toxin, the content of cGMP in cells sharply increases, which leads to the development of the phase of thrombocyte hypoaggregation.
Animals↗
Protective and other biological properties of Bacillus anthracis soluble antigens.
The soluble antigens were explored of the culture filtrate (CF) derived during static growth of B. anthracis vaccine strain 34F2 on a medium containing casein hydrolysate. Electrofocusing of CF preparations revealed that the protective activity was distributed over a wide range of pH 3-7. The most pronounced and stable protective activity was observed at pH 4.6-4.8. Following toxin factors were isolated and identified: protective antigen (87 kD), oedema factor (87 kD) and lethal factor (78-81 kD). The greatest protective activity was associated with antigens characterized by a molecular weight of 78-87 kD and toxic activity. Preparations of the oedema and lethal factors had the same protective activity as protective antigen (PA) preparations. Other CF soluble antigens protected about 30% of immunized guinea pigs. A protein was isolated with a molecular weight of 80 kD and isoelectric point at pH 5.3-5.7 which was not toxic and did not form toxic mixtures in association with other toxin factors; this protein featured a high immunogenic activity, however, it protected only 31% of immunized animals. Factors are analyzed which determine differences in the protective effects of live and chemical vaccines.
Animals↗
[The effect of lethal anthrax toxin on the functional activity of peritoneal mononuclear phagocytes and polymorphonuclear neutrophils in mice].
The mixture of purified protective antigen (PA) and the lethal factor (LF) of B. anthracis exotoxin in a dose incapable of causing cell damage inhibited the zymosan-stimulated luminol-dependent chemiluminescence of mononuclear phagocytes (MP) and polymorphonuclear neutrophils (PMN) in CBA mice and enhanced the chemiluminescence of PMN in BALB/c, CC57W and A/Sn mice. The conclusion is made that the capacity of mixture of PA and LF for the in vitro inhibition of stimulated production of active forms of oxygen in MP and PMN is directly related to the in vivo immunosuppressing activity of B. anthracis toxin. But the influence of the mixture of PA and LF on the production of active forms of oxygen in MP and PMN is not the leading factor of natural immunity to B. anthracis infection in mice.
Animals↗
[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.GPs rises in 1h 3.7 times and then falls below standard rate (5h). This is the evidence of the lungs antioxidant system potential power exhaustion. It has been established that in the liver, 4 times SOD activity increases in 2h after the toxin injection, and 1.5 times GP (tributyL) hydroperoxide) activity ascends in 1h. The ratio increase (150% for SOD/GP-H2O2 in 2h, 114% for GR/GP (tributyl hydroperoxide) and 61% for GR/GT in 5h) indicates the stable unbalance of this system. The pathogenetic significance of detoxication system disturbances in the lungs and liver tissues under the murine toxin influence is discussed.
Animals↗
[Prostaglandins and cyclic nucleotides in the dynamic development of an experimental poisoning syndrome caused by Yersinia pestis lipopolysaccharide].
This work deals with the influence of Y. pestis lipopolysaccharide (LPS), introduced intraperitoneally in a dose of 2 LD50, on the content of prostaglandins (PG), such as PGE, PGF2 alpha and 6-keto-PGF1 alpha, thromboxane, cAMP and cGMP in the liver, lungs and blood plasma of guinea pigs in the process of the development of experimental intoxication. The content of thromboxane in blood plasma increased 2.4-fold in 2 hours after intoxication and remained elevated for as long as 5 hours. Other parameters of blood plasma remained unchanged. The data obtained in this investigation indicate that thromboxane, known as a regulator of thrombogenesis, may induce early disturbances in microcirculation. A change in the content of PG was shown to occur in pulmonary tissue 2 and 5 hours after the beginning of intoxication. The content of PG in liver tissue was found to occur at a later period of the toxic action. The concentration of cyclic nucleotides (CN) in the tissues under study sharply increased even at the initial stage of the development of shock in guinea pigs. The effect of LPS on the metabolism of PG and CN, revealed in this investigation, resembles the effect produced by the thermostable fraction of "mouse" toxin.
Animals↗
[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. Glucagon content by 2-5 hour of shock was strong elevated. Proposal is made that Y. pestis mouse toxin might induce carbohydrate metabolism alterations via direct liver glucose synthesising enzymes inhibition rather than cAMP-dependent glycogenolysis and gluconeogenesis regulation disturbances in this organ.
Animals↗
[Purification and characteristics of a protective factor from Bacillus anthracis toxin].
It was found that during filtration of a sterile toxic cultural supernatant (TCS) obtained by 24 hour cultivation of the vaccinal strain through a column packed with porous glass or silochrome not only oedematic (OF) and lethal (LF), but also protective (PF) factors of toxin are adsorbed on the column. Elution of adsorbed antigens allowed for rapid concentration and purification of biologically active components of toxin from large volumes of TCS under conditions of limited proteolysis. The experimental results suggest that in 24 hour TCS and PF exists as large (87 kD) molecules as well as low molecular weight fragments whose molecular mass is of the order of 17-18 kD. The PF preparations whose molecular mass is below 68 kD possess a weak biological activity.
Animals↗
[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. The differences in metabolic effects between Yersinia pestis endotoxin and lipopolysaccharides of other Gram-negative bacteria are discussed.
Alprostadil↗
[Cyclic nucleotides in the dynamic development of shock caused by the murine toxin of Yersinia pestis].
The authors have studied the effect of Y. pestis "mouse" toxin (LD50), injected intravenously to rats, on cAMP and cGMP content in the tissues of different organs (the lungs, liver, heart, spleen, kidneys, small intestine) and in the blood in the course of the development of toxinfection shock. The effect of Y. pestis "mouse" toxin on cyclic nucleotide content in the organs of experimental animals is determined by the sum of oppositely directed effects produced by the thermostable and thermolabile fractions of the toxin. Its thermostable fraction, when introduced in the dose used in the experiments, did not kill the animals. The most pronounced changes in the cyclic nucleotide content have been detected in the lungs which appear to be the main target organ for Y. pestis "mouse" toxin.
Animals↗
[Relation between glycoprotein synthesis and carbohydrate metabolism in the small intestine mucosa. Effect of cholera enterotoxin].
The regulatory properties of adenylate cyclase in small intestinal mucosa were investigated. Glucagon, epinephrine and isoproterenol failed to activate the cAMP synthesis; prostaglandin E1 caused a 2.8-fold, while cholera toxin-a 4.5-fold stimulation. The latter was not able to increase the rate of glucose synthesis from alanine in vitro, but increased markedly the in vivo incorporation of 14C-labeled alanine into the mucus glucosamine. Unlabeled glucosamine excretion was also enhanced 3-fold. This provides evidence for the involvement of glycolysis and gluconeogenesis enzyme systems in the mucosal glycoprotein synthesis. It was assumed that both metabolic pathways may play a common physiological role, namely, to convert carbohydrates and gluconeogenic precursors into the substrate for glucosamine synthesis which is thought to be a rate-limiting step in small intestinal mucus secretion.
Adenylyl Cyclase Inhibitors↗
[Effect of cholera enterotoxin on carbohydrate metabolism of the liver and small intestine mucosa in the rabbit].
Changes in carbohydrate metabolism were studied in the isolated intestinal loops of rabbits during secretory diarrhea, induced by cholera enterotoxin. Glucose synthesis level in the small intestinal mucosa and liver was measured by isotope technique, using L-alanine as a precursor. Intestinal gluconeogenesis, calculated per mg of protein, appeared to be twice higher than in the liver of fasting rabbits. Cholera enterotoxin administration enhanced gluconeogenesis in the liver by 60%, as compared to the control. The rate of glucose synthesis and glucose-6-phosphatase activity in the intestinal mucosa remained unchanged, whereas glucose-6-phosphatase in the liver was slightly inhibited. It is suggested that gluconeogenesis in the liver supplies glucose as a convenient energy source for the secretory process induced by cholera enterotoxin in the rabbit small intestine.
Animals↗
[Carbohydrate metabolic disorder in experimental secretory diarrhea induced by cholera toxin].
Cholera toxin induced a massive mucus accumulation and a significant enhancement of arteriovenous difference in glucose concentration in the isolated loop of rabbit small intestine. Mucus hexosamine secretion increased threefold, whereas mucous lactate level remained unchanged. It is suggested that intensive mucus secretion is ensured by significant amounts of blood glucose, whose level is 65% increased, possibly due to the observed 1-6-fold liver gluconeogenesis acceleration. Though the mechanism of the latter is not yet known, the data obtained provide evidence that this stimulation is not cAMP-dependent.
Animals↗