[Proliferation and death of liver mononuclear cells in immune lesions induced by concanavalin A and anti-liver antibodies in mice].

Two types of experimental liver failure in mice were investigated to study the immune mechanisms of liver disease: 1) T-cell-mediated injury induced by administration of concanavalin A (ConA) and 2) antibody-mediated injury induced by administration of anti-liver antibodies (ALA, gamma-globulin fraction of sera from rabbits immunized with liver tissue). It was established, that both types of liver injury were accompanied by the activation of immune processes in the liver, as shown by the increase of liver mononuclear cell proliferation, estimated using IPO-38 monoclonal antibodies. In contrast to ConA treatment, the immune activation under ALA-treatment was also associated with the increase in the percentage of plasma cells and small lymphocytes in liver mononuclear cells.

[Functional activity of the peritoneal macrophages in mice with concanavalin A-induced hepatitis].

Hepatitis of T-cell genesis, a model of autoimmune damage of human liver, was caused in mice of CBA line by concanavalin A (Con A). The damage of liver was examined by activities of transaminases (alanine aminotransferase, aspartate aminotransferase) and alkaline phosphatase in mice blood plasma. Functional activity of macrophages in peritoneal fluid was studied by examination of phagocytosis of latex particles and oxygen--dependent metabolism (nitro-blue-tetrazolium- test).

[The role of nitric oxide in the development of humoral immune response in mice].

The immune response in CBA mice was evoked by injection of sheep erythrocytes. The number of antibody-producing cells in the spleen, as well as nitric oxide production, oxygen-dependent metabolism and 5"-nucleotidase activity of peritoneal macrophages and lymphocytes were studied on days 1-5-14 after immunization. It was shown that during the inductive phase of the immune response (day 1), the peritoneal cells increased nitric oxide production, while later their functional activity increased and NO level became normal.

[Effect of inhibitors of cyclooxygenase and lypoxygenase pathway of metabolism of arachidonic acid on the development and suppression of the immune response in mice].

The influence of indomethacin (IM) and nordihydroguaiaretic acid (NDGA) as inhibitors of cyclooxygenase and lypoxygenase pathways of arachidonic acid metabolism, accordingly, on the development of the immune response (IR) to sheep red blood cells (SRBC), as well as on the formation and functional activity of the antigen-induced (by the tolerogenous dose of SRBC) T-suppressors (AITs) was studied. Investigation was carried out on mice of line CBA. The IR was estimated by quantity of antibody-forming cells in the mouse spleen.

[Exogenous L-arginine modulates mitochondrial and microsomal oxidation in acute and intermittent normobaric hypoxia].

It is known that protective effects of adaptation to intermittent hypoxia are mediated partly by stimulating of some mitochondrial and microsomal enzymes activity. Our objective was to investigate whether exogenous NO (L-arginine) or NO blocker (L-NNA) modulate mitochondrial and microsomal oxidation during acute hypoxia (AH) and intermittent hypoxic training (IHT). In control rats AH (inhalation of 7% O2, 30 min) provoked a decrease of ADP-stimulated liver mitochondrial respiration.

[Effect of inhibitors of cyclooxygenase and lipoxygenase pathways of arachidonic acid oxidation on the immune response and the activity of the monoxygenase system and lipid peroxidation in the spleen and liver in mice].

In experiments on CBA mice we studied an immune response (IR) to sheep red blood cells, the activity of monooxygenase system and lipid peroxidation (LP) in a spleen and a liver after administration of indomethacin (IND) and nordihydroguaiaretic acid (NDGA) as the inhibitors of cyclooxygenase and lypoxygenase pathways of oxydation of arachidonic acid consequently. We have found that the both inhibitors changed differently the intensity of IR during its development. IND and NDGA activate the accumulation of antibody-forming cells in the mouse spleen in a dose-dependent fashion at both the inductive and fading phases of IR.

[The effect of chenophalk on the liver function of intact animals and in experimental hepatitis].

Chenophalk (chenodeoxycholeic acid) was given to Wistar rats, including intact animals and those with chronic toxic hepatitis, in daily oral dose of 15 mg/kg body weight during 11 days. Chronic toxic hepatitis was induced by 7 subcutaneous injections of carbon tetrachloride (0.3 ml of 50% oil solution per kg body weight) each three days.

[Effect of antibodies specific to sarcolemma of cardiomyocytes in activity of 5-nucleotidase in rats].

Rabbit antibodies specific to sarcolemma of cardiomyocytes have been studied for their effect on activity of 5'-nucleotidase ecto-enzyme of the Wistar rat cardiomyocytes. It is shown that incubation of isolated plasma membranes of cardiomyocytes of rats (100 micrograms of protein) with the gamma-globulin fraction of antisarcolemmal cardial serum (gamma-ASCS, 20 micrograms protein) and with the gamma-globulin fraction of normal rabbit serum (gamma-NRS, 0.20 micrograms protein) promotes a decrease of the enzyme activity.

[Oxygen-dependent processes in the liver and immunologic reactivity of rats in chronic liver damage induced by carbon tetrachloride].

The chronic hepatitis in Wistar rats was induced by seven subcutaneous injections of carbon tetrachloride (0.3 ml of 50% oil solution per 1 kg of body mass) made each third day. It was shown that cytochromes P-450 and b5 content, demethylase activity in the liver microsomal fraction as well as the oxygen tension in the liver tissue were decreased, while lipid peroxidation was intensified.

[The effect of antimembrane testicular antibodies on Na+, K(+)-ATPase activity in the testicles of rats of different ages].

The effect of large and small doses of rabbit antibodies specific to plasma membranes of the rat testicle cells has been studied in the experiments on Wistar rats of three age groups (preadolescent--aged 20 days, puberal--aged 5-7 months and old--aged 24-26 months). It is stated that incubation of plasma membranes by IgG fraction isolated from antimembrane testicular serum (IgG-ATCSm) in a large dose (43 g of protein G per 125 g of protein of membrane fraction) caused statistically reliable inhibition of Na+, K(+)-ATPase activity in the membranes of testicle cells of puberal and old rats. Preadolescent rats exhibit only a tendency to decrease the activity of this enzyme.