Biomedical subjects

E V Rukavishnikova

Publications and source records attributed to E V Rukavishnikova.

5 recordsLinked to original sources

PubMed1995

Interaction of rat liver lysosomes with basic polypeptides.

In order to gain knowledge on the interaction of lysosomes with proteins, we have assessed the equilibrium densities of the lysosomal membrane and matrix markers after in vitro incubation of rat liver lysosomes with various polypeptides. The addition of basic polypeptides, polylysine or protamine, to the suspension of lysosomes brought about a profound alteration of lysosomal membrane, causing extensive leakage of lysosomal matrix enzymes. Electron microscopic observation revealed a remarkable aggregation of lysosomes by the basic polypeptides. Polyglutamic acid, an acidic polypeptide, did not produce such effect. ATP was found to stabilize lysosomes during incubation, particularly with basic polypeptides.

Animals↗

PubMed1992

Endocytosis by liver cells during suppression of intralysosomal proteolysis.

The lysosomotropic agent chloroquine is widely used as a specific inhibitor of intralysosomal proteolysis in isolated hepatocytes. It was shown that in vitro chloroquine reversibly inhibited purified cathepsins H, B, L in concentrations less than those observed inside lysosomes in vivo. However, administration of high doses of chloroquine to rats (30-50 mg/kg i.p. as a single or repeated injections) was followed by increased cathepsin D and cysteine proteinase activities, as well as other lysosomal enzymes. Chloroquine administration did not induce any changes of carbon particles phagocytosis by liver cells (macrophages); modifications of fluid-phase (125I-PVP uptake) and receptor-mediated endocytosis (125I-asialo-fetuin uptake) were noted. Chloroquine administered in vivo reproduced some symptoms of lysosomal storage diseases (especially during repeated drug administration).

Animals↗

PubMed1991

Effects of chloroquine on lysosomes and endocytosis by liver cells in vivo.

1. Chloroquine accumulation in rat liver after a single and repeated drug administration and lysosomal changes resembling some symptoms of lysosomal storage diseases were observed. 2. Repeated chloroquine treatment of rats resulted in increased activity of liver lysosomal enzymes acid phosphatase and beta-galactosidase and a significant enhancement of the activities of cathepsin D and cysteine proteinases were found. 3. No changes in the activity of liver macrophages (as assessed by the colloidal carbon clearance test) or in fluid-phase endocytosis of the marker 125I-polyvinyl-pyrrolidone by hepatocytes in vivo were found.

Acid Phosphatase↗

PubMedDate not supplied

[The effect of single and repeated administration of chloroquine on the activity of lysosomal proteinases in rat liver cells].

Effects of single and repeated injections of lysosomotropic agent chloroquine on lysosomal proteolytic activity and physico-chemical properties of rat liver lysosomes have been studied. Chloroquine was administered intraperitoneally to rats at a dose of 30 mg/kg of body mass. Osmotic properties, lysosomal enzymes activity and functional state of the system of mononuclear phagocytes were estimated. No alterations of colloid carbon clearance followed by a single dose of chloroquine administration were noted. Distinct alterations in osmotic properties, weak labilization of lysosomes and an increase in acid hydrolases activity were similar after single and/or repeated chloroquine administrations, whereas activation of cysteine proteinases and cathepsin D were most pronounced. Chloroquine accumulation by rat liver cells proved to be similar, but the drug excretion was longer after repeated injections. The lysosomal disorders noted were similar to those symptoms of lysosomal storage disease.

Animals↗

PubMedDate not supplied

[Elimination of asialoorosomucoid and its catabolism in liver of rats with toxic CCl4-induced cirrhosis].

Human 125I-acyaloorosomucoid was intravenously injected to male Wistar rats. Hepatic cirrhosis was induced by oily CCl4 solution (0.04 ml toxin per 100 g body weight, twice a week for 2 months). Cirrhosis was found not to prevent blood elimination of 125I-acyaloorosomucoid (t1/2 = 2.53 versus 2.50 in the control). Ten minutes after injection, there was 75.2% of the administered radioactive dose in the liver versus 77.1% in the control. The 60-minute hepatic elimination of substrate in rats with cirrhosis was even more intensive than in the control animals, which is in agreement with the high levels of acid-soluble radioactivity (for 10 minutes). By large, CCl4-induced hepatic cirrhosis did not lead to disturbances of the hepatocytic function aimed at endocytosis and catabolism of acyaloorosomucoid.

Animals↗