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Biomedical subjects

N P Lebkova

Publications and source records attributed to N P Lebkova.

At least 19 recordsLinked to original sources
PubMed2006

Intracellular changes in rat hepatocytes after intratracheal administration of highly dispersed silicon dioxide and uridine effects on these changes.

Rat hepatocytes were examined under electron microscope at early terms after intratracheal administration of highly dispersed silicon dioxide powder against the background of uridine treatment. Penetration of powder particles into hepatocyte cytoplasm, nuclei, mitochondria, and peroxisomes and development of bacteria in these cells were observed. Uridine reduced the destructive effect of powder on the organelles, increased glycogen content in hepatocytes, and inhibited the formation of capsulated bacterial forms in these cells.

Animals↗
PubMed2004

Ultrastructural and cytochemical changes in the respiratory compartment of the lungs in rats after combined treatment with fine silicon dioxide powder and uridine.

Electron microscopy and cytochemical study of alveolar tissue of rat lungs were performed at the early stage after intratracheal treatment with fine silicon dioxide powder. The preparation was administered to animals receiving or not receiving intravenous injection of uridine. Dust particles permeated the cytoplasm, mitochondria, and nuclei of cells in the air-blood barrier of the alveoli. Uridine decreased the severity of dust-induced damage to cells and increased intracellular glycogen content.

Animals↗
PubMed2000

[Current ideas of intracellular energy maintaining mechanisms in health and disease].

The paper presents the author's own findings and data available in the literature concerning the intracellular mechanisms of conversion of fatty acids to glucose and glycogen in mammalian and human tissues in health and in disease. This conversion is considered by the author to be a regular adaptive response that maintains energy homeostasis in oxygen deficiency.

Animals↗
PubMed1999

[The adaptational intracellular mechanisms regulating energy homeostasis during intermittent normobaric hypoxia].

Rats trained to intermittent normobaric hypoxia (INH) developed an increase of the glycogen contents in the heart and liver parenchymatous cells. Fatty acids seem to be the main source for synthesis of the intracellular glycogen. The intracellular transformation of the lipid energy substrate into the carbohydrates maintains the energy homeostasis in hepatocytes and cardiomyocytes during hypoxic intervals of the INH thus creating the necessary conditions. This kind of regulating the substance supply of the cell energy supports the organism stability under various effects.

Adaptation, Physiological↗
PubMed1991

[The substrate support for energy homeostasis in starvation].

Ultrastructural study of liver and leucocytes and biochemical study of the main fat and carbohydrate substrates of anergy metabolism were carried out in rats under full alimentary starvation. In vast prelethal period in the liver and probably in other organs the glucogenetic role of amino acids is increased in connection with expressed cells structure decomposition.

Animals↗
PubMed1987

[Effect of Eleutherococcus on the subcellular structures of the heart in experimental myocardial infarct].

The effect of Eleutherococcus on subcellular heart organization in rats with or without myocardial infarction was investigated. It was found that Eleutherococcus decreases ultrastructural lesions in the ischemic area, intensifies regeneration of subcellular structures and accelerates the recovery after myocardial infarction. The accumulation of glycogen, lipids and lysosomes is observed in lipocytes. It is suggested that positive effect of Eleutherococcus during myocardial infarction is related to lipid transformation into glycogen.

Animals↗
PubMed1985

[Subcellular localization of glycogen-UDP-glucosyltransferase in the hepatocytes of intact and fasting rats].

Electron microscope cytochemical techniques by Takeuchi et al. were used to study the localization of glycogen-UDP-glucosyl-transferase (GUDPG) in hepatocytes of intact and fasting rats. Glycogen was found in the cytoplasm, nuclei, mitochondria, microbodies and lysosomes of the hepatocytes of intact and fasting animals after special cytochemical procedures for determination of GUDPG.

Animals↗
PubMed1983

[Mechanisms of reversibility of fatty degeneration].

Carnitine acetyltransferase (CAT) was determined electron microscopically and histochemically in hepatocytes of patients with cholecystitis and in hepatocytes of fasting rats. In the latter, tests for this enzyme were also done in subcutaneous tissue. Glycogen was determined histochemically in thin sections of hepatocytes from intact rats. CAT was found in mitochondria, microbodies, lysosomes, and degenerating fat inclusions in hepatocytes and cytomembranes of adipocytes. Glycogen accumulations were found in fat inclusions. It was concluded that CAT played a role in resorption of excessive fat from which intracellular glycogen was formed. The myelin-like membrane structures remaining after utilization of fat from fat inclusions were eliminated from the cells and could penetrate into the adjacent capillaries.

Acetyltransferases↗
PubMed1983

[Subcellular localization of carnitine acetyltransferase in the organs of intact and starving rats].

Electron and histochemical techniques were used to study the localization of carnitine acetyltransferase (CAT) in different tissues of intact and fasting rats (at the 5th day after keeping the animals without food, with the drinking regimen remaining unchanged). The enzyme was discovered in mitochondria and microbodies of cardiomyocytes, hepatocytes and fibers of the skeletal muscle of intact rats. In fasting animals, CAT was identified not only in mitochondria and microbodies of cardiomyocytes and hepatocytes but also in membranes surrounding fat inclusions as well as in the plasmalemma of adipocytes. On fasting the content of microbodies in the cells was higher than that in normality.

Acetyltransferases↗
PubMed1982

[Lipid transformation into glycogen in animal and human cells].

On the basis of analysis of the literature and the author's data a hypothesis of transformation of lipids into glycogen in animal and human cells by means of microbodies and lysosomes as one of the universal adaptative reactions of the host is substantiated. In the opinion of the author, both microbodies and lysosomes may take part both in the process of oxidation of intracellular lipids up to intermediate metabolism products and in the process of glycogen synthesis from these products. As a result of enhanced oxidation and transformation of lipids into glycogen the energy of the cell improves and the possibility of development of fatty dystrophy decreases. The hypothesis is based on the structural association of microbodies, lysosomes, fatty and glycogen inclusions observed by the author in cells of various organs in different pathological processes, as well as on certain biochemical data.

Adrenal Glands↗
PubMed1981

[Structural and functional changes in the liver in chronic recurrent cholecystitis].

Destructive, inflammatory and sclerotic alterations of the hepatic tissue, increased content of lipid inclusions, lysosomes and microbodies in hepatocytes, vesiculation of the endoplasmic reticulum and depletion of ribosomal granules in it were revealed by morphological examinations of liver samples from the gall bladder bed from patients will rarely, frequently and continuously recurring chronic cholecystitis. A relationship between resorption of lipid structures, content of lysosomes and microbodies, and glycogen accumulation in hepatic cells was found. The destructive morphological changes correlated with reduced capacity of the liver to absorb radioactive label, an increase of alanine transaminase level in the blood, and decreased oxidative processes in the mitochondrial fraction of the liver. The results of the study attest to the involvement of the liver in the pathological process in accord with the rate of cholecystitis recurrency.

Biopsy↗
PubMed1980

[Ultrastructural manifestations of early metabolic disorders in the myocardium of dogs with alloxan diabetes].

The ultrastructure of dog cardiomyocytes was studied one month after reproducing alloxan diabetes, with respect to myocardial extraction from the blood of glucose, nonesterified fatty acids, beta-lipoproteins and ketone bodies as well as to respiration in conjunction with oxidative phosphorylation of mitochondria, hexokinase and phosphorylase activity. Destructive changes in mitochondria, increased glycogen content in cardiomyocytes were revealed in the absence of glucose consumption by the myocardium which absorbed only lipoid metabolites. Lipoid inclusions were rarely seen in cardiomyocytes. The myocardium showed the increased content of lysosomes and hydrolytic phosphorylase. It is suggested that lipoid metabolites transform to glycogen, with lysosomes participating in the process.

Alloxan↗