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D K Novikov

Publications and source records attributed to D K Novikov.

At least 37 records · Page 2Linked to original sources
PubMed1990

[The effect of khellin and timefurone on secretion and catabolism of lipoproteins by cultured human and rabbit hepatocytes].

Using human and rabbit hepatocyte cultures, the effects of khellin and timefurone on lipoprotein metabolism were studied with special reference to the following parameters: i) binding and degradation of 125I-labeled low density lipoproteins (LDL); ii) apoprotein B (apo-B) secretion measured by immunoenzymatic assay, iii) [35S]methionine labeled apo-B and apo-E within the composition of very low density lipoproteins (VLDL); iiii) total cholesterol synthesis and cholesterol secretion within the composition of VLDL. The therapeutic concentrations (0.1-10 micrograms/ml) of the above drugs had no appreciable effect on the binding and degradation of 125I-LDL but inhibited the secretion of apo-B VLDL, leaving the apo-E VLDL unaffected. This was paralleled with inhibition of cholesterol synthesis (by 30-50%) and VLDL secretion. These results suggest that khellin and timefurone mediate the hypolipidemic effect via the reduction of the intracellular synthesis of cholesterol and secretion of apo-B containing VLDL by hepatocytes.

Animals↗
PubMed1989

Lipopolysaccharide toxin can directly stimulate the intracellular accumulation of lipids and their secretion into medium in the primary culture of rabbit hepatocytes.

Low doses (0.1-0.3 micrograms/ml per 10(6) cells) of the lipopolysaccharide toxin (LPS) from Salmonella typhimurium were shown to increase (after an 18 h incubation) the intracellular content of free cholesterol (CH), esterified cholesterol (EC) and triglycerides (TG) by 30-40% in the primary culture of rabbit hepatocytes. A similar increase was found for the incorporation of [14C]acetate into these lipids. The concentration of lipids in cultural medium, under these conditions, was also augmented: by 30-40% for CH; by 50-60% for TG and by 60-80% for EC. Higher doses (up to 50 micrograms/ml) of LPS hardly affected the lipid content in hepatocytes but strongly (by two-fold) inhibited the secretion of lipids. It is suggested that in vivo low concentrations of LPS in bloodstream (in the absence of conspicuous pathology) might induce hyperlipidemia directly influencing on hepatic cells, while, under the higher concentrations of LPS, hyperlipidemia caused by cachectin (or tumor necrosis factor) is probably observed.

Animals↗
PubMed1989

Very low density lipoprotein secretion by cultured hepatocytes of rabbits fed purified or autoxidized cholesterol.

The main objectives of this study were to compare the effects of dietary commercial cholesterol (containing 5% of oxidized cholesterol derivatives) and purified cholesterol on the secretion rate of very low density lipoprotein apolipoproteins and lipids by cultured rabbit hepatocytes and to verify the hypothesis that products of cholesterol autoxidation stimulate the rapid development of hypercholesterolemia. Rabbits fed dietary (old) commercial cholesterol for six weeks showed a fivefold increase in the serum concentration of cholesterol compared with that in purified cholesterol-fed rabbits. The secretion rates of very low density lipoprotein total protein and very low density lipoprotein [3H]apolipoproteins were similar for the hepatocytes of these two cholesterol-fed groups of animals and were two- and threefold greater, respectively, than for cells from control rabbits. Cholesteryl ester content of the hepatocytes from dietary (old) commercial cholesterol-fed rabbits was dramatically increased in comparison with hepatocytes from control and purified cholesterol-fed rabbits. The elevated intracellular cholesteryl ester content is assumed to account for such an increase of very low density lipoprotein-cholesteryl ester secretion by cells prepared from dietary (old) commercial cholesterol-fed rabbits. These effects appear to be caused by activation of cholesterol esterification by oxidized cholesterol derivatives. The rapid development of hypercholesterolemia induced by dietary (old) commercial cholesterol is associated, at least in part, with the stimulated production of hepatic very low density lipoprotein apolipoproteins and cholesteryl esters.

Animals↗
PubMed1989

[Secretion of very low density lipoproteins by cultured rabbit hepatocytes with hypercholesteremia, induced by purified cholesterol and containing autooxidation products].

To evaluate the impact of oxidized derivatives of cholesterol on the development of hypercholesterolemia in rabbits, the secretion of very low density lipoprotein (VLDL) apoproteins and lipids was studied in cultures of hepatocytes obtained from: i) control rabbits, ii) rabbits fed on purified cholesterol (PCH), and, iii) rabbits fed on old commercial cholesterol (OCH) containing 5% of oxidized cholesterol derivatives. The rabbits fed on OCH for 6 weeks revealed a 5-fold increase in the serum cholesterol level compared with that in PCH-fed rabbits. The secretion of VLDL apoproteins and lipids by hepatocytes of two cholesterol-fed groups was similar, but was 2-3 times as high as that of cells from control rabbits. The cholesterol ester content in hepatocytes and the secretion of VLDL cholesterol esters by hepatocytes from OCH-fed rabbits was dramatically increased in comparison with hepatocytes from control and PCH-fed rabbits. These effects appear to be caused by the activation of cholesterol esterification by oxidized cholesterol derivatives. The rapid development of hypercholesterolemia in OCH-fed rabbits is at least partly associated with the stimulation of hepatic VLDL production.

Animals↗
PubMed1988

VLDL apoprotein secretion and apo-B mRNA level in primary culture of cholesterol-loaded rabbit hepatocytes.

Incubation of cultured rabbit hepatocytes with beta very low density lipoproteins (beta-VLDL) induces a dose-dependent increase in cell cholesterol (CH) content and VLDL apoprotein (apo) B and E secretion without change in apo-B mRNA level. These data suggest that beta-VLDL may exert a stimulatory effect on hepatic apo-B production at the co-translational and/or posttranslational level.

Animals↗
PubMed1987

Effect of bezafibrate on lipoprotein secretion by cultured human hepatocytes.

The secretion of newly synthesized very low density lipoprotein and low density lipoprotein (VLDL + LDL) and high density lipoprotein (HDL) in cultured human hepatocytes in the presence or absence of bezafibrate added to the culture medium has been evaluated. The content of triacylglycerol, apolipoprotein B, 3H-labeled proteins and 14C-labeled lipids accumulated in a culture medium increased linearly for periods up to 18 h. During incubation, cellular triacylglycerol content was unchanged. This hypolipidemic agent, at a concentration of 10 microM, inhibited secretion of the several VLDL + LDL [3H]apolipoproteins and the VLDL + LDL [14C]lipids, suggesting it can affect the processes of biosynthesis and secretion. The secretion of total [3H]apolipoproteins in the HDL fraction and [3H]protein (d greater than 1.21 g/ml) was unchanged after an exposure to bezafibrate (10 microM). Incubation in the presence of 10 microM bezafibrate resulted also in decreases in both total VLDL neutral lipids and apolipoprotein B secreted into the medium. These results indicate that bezafibrate might exert its plasma lipid-lowering effect by suppressing the VLDL production in liver and reducing the secretion of VLDL into the circulation.

Bezafibrate↗
PubMed1987

[Effect of staphylococcal toxin on lymphocyte receptors and function].

Staphylococcal toxin at a concentration of 10(-3) inhibits in vitro the rosette-formation of lymphocytes, taken from healthy donors and patients with purulent septic diseases, with sheep and mouse red blood cells, changes the ratio of lymphocyte subpopulation, modifies the spontaneous antigen- and mitogen-dependent migration of leukocytes. The latter phenomenon is not linked with disturbances in the lymphokine-producing activity of lymphocytes, but results from changes in the migration properties of granulocytes.

B-Lymphocytes↗
PubMed1986

[Effect of bezafibrate on lipoprotein secretion by cultured human hepatocytes].

The rate of synthesis and secretion of lipid and apoprotein components of lipoprotein fractions and of proteins of the nonlipoprotein fraction d greater than 1.21 g/ml by human hepatocytes in culture was determined. The cells were incubated for 18 hours in the media containing [14C] acetate or [3H]-marked leucine in the presence of bezafibrate or without it. VLDL, HDL and d greater than 1.21 g/ml fractions were separated by differential ultracentrifugation. The lipids were divided using thin-layer chromatography, and the apoprotein-using SDS-electrophoresis in polyacrylamide gel. Bezafibrate in the therapeutic concentration of 10 microM specifically inhibits apoprotein and VLDL lipid secretion. Lowered secretion of all VLDL apoproteins was revealed, which points to a decrease in the number of secreted particles. The effect of bezafibrate was found to be associated with the inhibition of the intracellular synthesis of lipids. The secretion of HDL proteins and of d greater than 1.21 g/ml fraction proteins was unchanged with 10 microM of bezafibrate.

Adult↗
PubMed1983

[Effect of tumor antigens on leukocyte adherence in the blood in stomach cancer].

The reaction of changes in leukocyte adherence was compared in 79 cases of stomach cancer, 44 cases of other gastric diseases and healthy subjects. Tumor antigens were shown to inhibit the adherence of lymphocytes and granulocytes in 61 out of 79 cancer patients (77,2%); adherence inhibition was more frequently observed in patients with stage I-III tumors than in cases of stage IV tumors. The removal of the antigens of normal mucosa from tumor tissue extracts did not affect the frequency of positive reactions in cancer patients significantly. However, the frequency dropped from 22-34 to 2.3-13.6% in the group of non-tumor patients.

Adult↗
PubMed1983

[Effect of tumor antigens on receptors of T-and B-lymphocytes in patients with cancer of the stomach].

The effect of tumor antigens and those of gastric mucosa on rosette-formation by T-lymphocytes of blood and sheep red blood cells was studied in 65 gastric cancer patients by means of a spontaneous E-rosette-formation variation test. Antigens of original tumor extracts stimulated rosette-formation in 55.4% of patients, more frequently in cases of stage I-II tumors than in those of stage IV. After antigens of normal mucosa were removed from tumor extracts the frequency of positive tests did not change significantly in gastric cancer group, whereas, in controls, it dropped from 26.4 to 7.5%. Tumor antigens tested did not produce the same effect on the rosette-formation by B-lymphocytes with mouse red blood cells.

Animals↗
PubMed1981

[Determination of leukocyte sensitization to tumor and embryonic tissue antigens in cancer of the large intestine].

Aqueous-saline extracts of autologous rectal tumor tissue inhibited leukocyte migration in 7 out of 10 patients with rectal tumors in autoplasm-containing medium, and in 5 out of 11 patients-in control serum. Antigens of allogenic rectal tumors inhibited leukocyte migration (LMI) in 4 out of 5 patients (stage II), in 15 out of 21 patients (stage III), and in 5 out of 10 patients (stage IV) in control serum medium, and in non of control patients. Leukocyte sensitization to mucosal antigen was established only in 8% of patients (stage II-IV), in control serum medium. LMI in medium containing autoplasm and control serum was observed in 24 out of 36 patients. Extracts obtained from human embryonal liver inhibited leukocyte migration in 14 out of 27 patients (stage II-IV), including 3 cases in which leukocytes did not respond to tumor-associated antigen. LMI by carcinoembryonic antigen was registered in a total of 31 out of 36 cases (86%). In 5 cases out of 7, unresponsive leukocytes of patients with rectal tumors did respond to tumor-associated antigen by inhibiting leukocyte migration, after re-incubation at low temperature, in a medium free from autologous blood plasma.

Adenocarcinoma↗