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Biomedical subjects

V Nikolaev

Publications and source records attributed to V Nikolaev.

11 recordsLinked to original sources

Deliganded albumin as a liquid adsorbent in the treatment of burn toxemia.

A new generation of synthetic carbon adsorbents was used in production of deliganded human serum albumin preparation. Thermal effects of officinal and deliganded albumin interaction with specific chemical markers were analyzed by flow microcalorimetry. The results demonstrated a 2.5-fold increase of the complexing ability for the deliganded one. The detoxifying potentials of deliganded albumin were studied in comparison with officinal preparation in rats with burn toxemia after IIIB-IV degree thermal injury and in model experiments with blood serum of patients after severe thermal burn. The transfusion of a 5% officinal albumin solution in rats 1 h after burn trauma resulted in a decrease of serum and liver cytosols cytotoxicity 2.2 and 2.4 times, respectively, in comparison with those of burned rats. After deliganded albumin transfusion the cytotoxic activity of blood serum dropped 8.5 times and that of the liver cytosols 18.5 times. The incubation of blood serum of injured patients with equal amounts of a 5% solutions of officinal or deliganded albumin resulted in a fall of the cytotoxicity level and the growth of binding ability. A comparative analysis of detoxifying potentials of albumin preparations has unambiguously demonstrated deliganded albumin advantages.

Adsorption↗

Staphylococcus aureus causing osteomyelitis binds to a nonapeptide sequence in bone sialoprotein.

Bone sialoprotein is a glycoprotein of the bone and dentine extracellular matrix. This protein consists of 320 amino acids, of which 25% are glutamic and aspartic acid residues. Sialic acid, containing oligosaccharides and tyrosine sulphate residues, supplies additional polyanionic properties. Staphylococcal cells, isolated from patients suffering from infection of bone tissue, bind the bone-derived sialoprotein, an interaction which is specifically inhibited by the recombinant bone sialoprotein core protein. We have previously shown that the 150 N-terminal amino acid residues of bone sialoprotein are responsible for the binding to staphylococcal cells. By using recombinant deleted variants of bone sialoprotein and synthetic peptides, we have now localized the staphylococcal binding site to less than 10 residues within the N-terminal part of the protein.

Amino Acid Sequence↗

Biophysical studies on the correction of uremic human serum albumin binding defects by in vitro charcoal adsorption treatment.

Spectrofluorimetry, flow microcalorimetry, and differential scanning microcalorimetry (DSMC) were used to study the conformation, binding function, and ligand loading of uremic albumin obtained from the blood plasma of 2 end-stage renal disease (ESRD) patients before and after charcoal plasma treatment at different pH values (3.0-9.0). The spectrofluorimetric patterns of conformational N-F transition at low pH (4.2-3.5) are practically identical for both samples of uremic human serum albumin (HSA) and control HSA from healthy donors. After the charcoal treatment at pH 3.0 and 4.0, the enthalpies of complexing on uremic HSA with bromsulfalein and sodium dodecylsulfate approach that of donor HSA. The binding affinity of uremic HSA for sodium octanoate, phenol red, and salicylic acid following low pH charcoal treatment even exceed those of donor HSA. At the same time the charcoal treatment of uremic plasma at neutral and alkaline pH does not notably improve the binding characteristics of isolated HSA. Adsorption at low pH values completely restores the tryptophan fluorescence spectrum position of uremic albumin and improves the thermodynamic characteristics of its melting process. Using DSMC data, it can nevertheless be concluded that some conformational changes or a certain amount of high-affinity bound endogenous ligands still remain after low pH uremic HSA purification. The latter conclusion requires additional improvements of adsorption treatment of uremic plasma.

Adsorption↗

Some characteristics of new DNA-bearing plasmoimmunoadsorbents based on fibrous activated carbon.

A new dual adsorbent containing from 1 to 8 mg of native or denatured thymic DNA per 1 g of the fibrous activated carbon matrix has demonstrated sufficient biocompatibility and good selectivity for DNA-binding plasma substances. At the same time, this dual adsorbent exhibits a full scale of coupling modalities characteristic of the highest quality activated carbons. All these features of DNA-coated fibrous activated carbons allow them to be considered as promising plasmosorbents for the treatment of numerous immuno-dependent diseases and metabolic disorders.

Biocompatible Materials↗

Stereochemical nature of the products of linoleic acid oxidation catalyzed by lipoxygenases from potato and soybean.

When linoleic acid was incubated with the purified potato lipoxygenase under O2 atmosphere, a mixture of 9 and 13-hydroperoxyoctadecadienoic acids was formed. Stereochemical analysis of the respective methyl-hydroxyoctadecadienoic acids revealed that the 9-isomer was in S-configuration whereas 13-hydroxyoctadecadienoic acid was a mixture of S (39%) and R (61%). Exactly the opposite was the case with the soybean lipoxygenase products, where the 13-isomer was found to be in S-configuration and 9-hydroxyoctadecadienoic acid - a mixture of S (73%) and R (27%). A general scheme is proposed for the stereochemical nature of oxidation products of enzymes which are predominantly either [+2] or [-2] lipoxygenases.

Chromatography, High Pressure Liquid↗

Biochemical changes in the rat after chronic thioacetamide intoxication.

Male Wistar rats were given drinking water ad libitum with 0.075% thioacetamide (TAA) for 4 weeks. TAA treatment did not affect serum aminotransferase activities and total bilirubin content. The activities of 5'-nucleotidase, K+, Na+- and Mg2+-adenosine triphosphatases in liver plasma membrane preparations were strongly depressed, while that of gamma-glutamyl transferase was considerably increased. A decline in liver microsomal cytochrome P-450 and cytochrome b5 concentrations was also recorded. In contrast, the content of reduced glutathione in liver homogenate supernatant (9000 g) increased about 2-fold. As plasma membrane associated enzymes seem to be exclusively affected, the liver plasma membrane could be involved in the pathogenesis of the TAA-induced precirrhotic liver changes.

Acetamides↗

Biochemical changes in alpha-naphthyl isothiocyanate-induced chronic cholangitis in the rat.

Male Wistar rats were treated for 3 weeks with alpha-naphthyl isothiocyanate (ANIT, 5.4 mmol per kg food). Chronic necrotic cholangitis without pronounced transaminasemia and hyperbilirubinemia developed. The activity of 5'-nucleotidase in liver plasma membrane preparations was strongly depressed (3.5 times) while the activities of K+-, Na+- and Mg++-ATPases were not affected. The liver microsomal cytochrome P-450 and cytochrome b5 contents decreased. Elevation of reduced glutathione liver content after challenge with ANIT was recorded. The observed biochemical changes may be important for the pathogenesis of ANIT-induced chronic cholangitis.

1-Naphthylisothiocyanate↗

Interaction between glucose diet and ethanol on rat liver microsomal induction and liver plasma membrane damage in chronic hexachlorobenzene intoxication.

Male Wistar rats fed for 60 days a glucose diet containing 17.5 mmol hexachlorobenzene/kg show a less pronounced increase in serum parameters and microsomal cytochrome P-450 concentration and a lower decrease in liver plasma membrane 5'-nucleotidase, K+, Na+- and Mg++-adenosine triphosphatase activities than the controls fed standard diet + hexachlorobenzene. Addition of 10% ethanol to the drinking water eliminates the "glucose effect". The glucose diet and ethanol exert contrasting effects on microsomal enzyme induction and liver plasma membrane damage in hexachlorobenzene intoxication.

Animals↗

[Effect of prior starvation on the development of acute thioacetamide-induced liver damage in rats].

The effect of previous fasting on the liver morphological changes and microsomal cytochrome P-450 and b5 content was studied in thioacetamide-induced (100 mg/kg) rat liver necrosis. Starvation for 48 hours immediately before thioacetamide administration aggravates the dystrophic and necrotic processes, as revealed by histology, electron microscopic investigations and serum aminotransferase activity. The liver microsomal cytochrome P-450 concentration tended to decrease after thioacetamide challenge, with fasting resulting in a more significant loss of cytochrome P-450. Cytochrome b5 content, however, was found to increase in acute liver necrosis induced by thioacetamide.

Acetamides↗

The effect of thioacetamide on rat liver plasma membrane enzymes and its potentiation by fasting.

Thioacetamide, given intraperitoneally (1.4 mmol/kg body mass) to male Wistar rats 24 h before sacrifice promoted a marked elevation of serum aminotransferases, loss of microsomal cytochrome P-450 content and a significant reduction (about 50%) of the liver plasma membrane enzymatic activities (5'-nucleotidase; K+, Na+- and Mg2+-adenosine triphosphatases; and gamma-glutamyl transferase). Previous starvation for 48 h, immediately prior to thioacetamide administration, strongly potentiated the effects of thioacetamide on the serum, microsomal and liver plasma membrane parameters, while fasting itself did not affect them. The liver plasma membrane damage may be one of the reasons for the cell death in thioacetamide-intoxicated rat livers.

Acetamides↗

Rat liver plasma membrane damage in hexachlorobenzene intoxication and its potentiation by ethanol.

Chronic feeding of male Wistar rats with food containing hexachlorobenzene (HCB) at 17.5 mmol/kg induced elevation of serum amino-transferases and bilirubin content, increase of microsomal cytochrome P-450 concentration, and decrease of 5'-nucleotidase, K+,Na+- and Mg2+-adenosine triphosphatase activities in liver plasma membrane preparations. These changes were potentiated by ethanol consumption suggesting a possible role of liver plasma membrane damage in the pathogenesis of HCB intoxication.

Alanine Transaminase↗