Analysis of General Toxicity of Ergoferon.

For antibody-based drugs, it is important and relevant to study their toxic effects, which can often become limiting when prescribing this type of therapy. General toxicity of antiviral drug Ergoferon based on technologically processed antibodies was studied on sexually mature animals. Analysis of acute toxicity showed the absence of lethal outcomes when the drug was administered to adult rats at the maximum tolerated doses. In a study of repeated dose toxicity, no adverse effects of the drug were detected.

[A new approach to the determination of glycogen concentration in various tissues and comments on the interpretation of its results].

A simple specific method for the detection of glycogen concentration in various tissues without disintegration of its structure is described. The method includes staining of glycogen molecules with iodine. The results of determination do not depend on the presence of polysaccharides because they are not stained with iodine but release reducing sugars during hydrolysis. Glycogen content is calculated from the calibration curve.

[Effect of ethanol on the results of determination of metabolic parameters, enzymatic activity, and certain hormones in the blood serum].

The authors report data demonstrating the in vitro influence of 0.3-6 per thousand ethyl alcohol on the results of determination of metabolic parameters, enzymatic activity, and certain hormones in the blood serum. It is shown that ethyl alcohol may change results of immunoenzyme assays used for kinetic determination of enzyme activities and metabolites.

Immunoprotective effects of prolactin during stress-induced immune dysfunction.

We showed for the first time that prolactin stimulates the synthesis and release of immunomodulating cytokines and lymphocyte-activating factors (e.g., interleukin-1) by peritoneal macrophages. Prolactin abolished the stress-induced inhibition of proliferation of peripheral blood lymphocytes and increased cell sensitivity to regulatory effects of interleukin-1 in the reaction of lymphocyte blast transformation. These data illustrate the mechanism of immunoprotective activity of prolactin during stress.

[Effect of prolactin on the level of corticosterone in the blood and synthesis of lymphocyte-activating factors by macrophages under conditions of glucocorticoid loading]. / Deistvie prolaktina na uroven' kortikosterona v krovi i sintez makrofagami limfotsit-aktiviruiushchikh faktorov v usloviakh gliukokortikoidnoi nagruzki.

The present study examines in vivo the interaction between glucocorticoids and prolactin, and immunomodulating activity of prolactin, including prolactin-induced changes in production of lymphocyte-activating factors and alteration in humoral immune response. It was shown that prolactin application increased the level of corticosterone in the rat blood. Administration of prolactin prior to hydrocortisone administration induced alteration in the level of corticosterone that depended on the dose of hydrocortisone. Application of hydrocortisone reduced humoral immune response and lymphocyte-activating factors production by peritoneal macrophages. Administration of prolactin prior to hydrocortisone administration prevents inhibitory action of glucocorticoids/on humoral immune response and lymphocyte-activating factors production by macrophages.

[Glucocorticoid hormones in immunomodulating effect of defensins]. / Gliukokortikoidnye gormony v realizatsii immunomoduliruiushchego deistviia defensinov.

Defensins are a family of antimicrobial cationic peptides localized mainly in neutrophile granulocytes. The defensins are known to display corticostatic activity by means of suppression of stress- and ACTH-induced rise in corticosterone level in the blood. The present study examines influence of defensin fractions with different corticostatic activity on suppressor functions of T-lymphocytes. It was shown that corticostatic effects of defensins are revealed under an increased level of glucocorticoids in the blood after hydrocortisone application. Defensins were found to limit the inhibitory action of glucocorticoids on the suppressor functions of T-lymphocytes. After adrenalectomy this phenomenon was not observed.

[Modulation by tauroursodeoxycholic acid of proliferation of the rat ischemic liver hepatocytes]. / Moduliatsiia tauroursodezoksikholevoi kislotoi proliferatsii gepatotsitov ishemizirovannoi pecheni krys.

The influence of the tauroursodeoxycholic acid (TUDCA) on hepatocyte proliferation after 180-minute ischemia of rat liver was investigated. TUDCA in a dose of 200 mg/kg did not change hepatocyte proliferation in the liver of intact rats and had no cytotoxic effect. The preliminary introduction of TUDCA accelerated regenerative processes in the liver in the postischemic period possibly due to synchronization of hepatocyte division. The membrane stabilizing effect of TUDCA manifested in reduction of the liver enzyme activity in blood serum was found.

Effect of bile acids on the proliferative activity and apoptosis of rat hepatocytes.

Bile acids are known to have damaging as well as protective effects on liver cells. A likely candidate for bile acid-mediated hepatocellular injury during cholestasis is glycochenodeoxycholic acid (GCDCA), a hydrophobic bile acid with a direct cytotoxic effect on hepatocytes. In contrast, ursodeoxycholic acid was shown to exhibit protective effects. Our aim was to determine the effect of GCDCA on proliferation, synthesis and secretion of proteins and death processes in cultured rat hepatocytes. Furthermore, it should be studied whether the hydrophilic bile acid tauroursodeoxycholic acid (TUDCA) might be able to protect cells from the damaging effect of GCDCA. Our results demonstrate that GCDCA decreased dose-dependently hepatocellular proliferation, synthesis and secretion of newly synthesized proteins and, at low concentration, induced apoptosis or, at high doses, cytolysis of cultured hepatocytes. TUDCA did not exert cytotoxic effects on the isolated hepatocytes at a wide range of concentrations. However, TUDCA coincubated with GCDCA protected the cells from the damaging effect of GCDCA at all measured parameters except the secretion of newly synthesized protein.

[Effects of bile acid preparations on DNA biosynthesis, apoptosis, and necrosis in hepatocytes in vitro]. / Vliianie preparatov zhelchnykh kislot na biosintez DNK, apoptoz i nekroz gepatotsitov in vitro.

Using primary culture of hepatocytes it was shown that glycochenodeoxycholic acid (GCDCA) in a dose dependent manner induces apoptosis or necrosis of the hepatocytes and inhibits DNA biosynthesis. Ursodeoxycholic acid (UDCA) and tauroursodexycholic acid (TUDCA) do not cause apoptosis or necrosis of the hepatocytes in a range of doses 25-400 micrograms/ml. But in the presence of GCDCA both preparations have an antiapoptosogenic effect and TUDCA has also an antinecrosogenic effect.

Effect of polyunsaturated phosphatidyl-choline on lipid transport system in alcoholic liver injury.

The aim of this study was to determine whether serum lipid composition and lipolytic activities in alcoholinduced liver dystrophy were modified by the co-administration of polyunsaturated phosphatidylcholine (PPC). Chronic alcohol intoxication was induced in rats by intragastric ethanol administration of 3.5 g/kg body weight per day over 56 days. Aqueous PPC suspension was given intragastrally in doses of 100 and 300 mg/kg body weight. Chronic alcohol intoxication led to the development of protein and lipid dystrophy of hepatocytes. PPC partially prevented alcoholic injury of the liver cells and had a normalizing effect on cholesterol esterification, lipolysis of lipoproteins and on the fatty acid composition of the main lipoprotein classes.