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Biomedical subjects

L A Aleksandrova

Publications and source records attributed to L A Aleksandrova.

At least 19 recordsLinked to original sources
PubMed2004

Natural antioxidant L-carnosine inhibits LPO intensification in structures of the auditory analyzer under conditions of chronic exposure to aminoglycoside antibiotics.

Intragastric administration of L-carnosine suspension to Wistar-Kyoto rats 3 days before and after 7-day course of intraperitoneal injections of ototoxic aminoglycoside antibiotic kanamycin compensated expenditures of tissue antioxidant systems and significantly eliminated kanamycin-induced intensification of MDA production in tissues of the membrane part of the cochlea and in the auditory cortex of the temporal lobe. L-NAME (competitive NO synthase inhibitor) also inhibited LPO, increased total antioxidant activity, and decreased ototoxicity of kanamycin, which confirms the contribution of NO into LPO intensification under conditions of aminoglycoside treatment. Inhibition of pathological intensification of LPO processes and increase in total antioxidant activity under conditions of induced acute aminoglycoside ototoxicity characterizes L-carnosine as a highly effective otoprotector.

Animals↗
PubMed2004

Protective effect of carnosine on excitable structures of the auditory apparatus in albino rats with acute acoustic trauma.

We studied the effect of natural antioxidant carnosine on Wistar rats with experimental acoustic trauma of the auditory apparatus. Repeated intraperitoneal injection of carnosine in a dose of 200 mg/kg 12 and 0.5 h before modeling of acute acoustic trauma decreased the severity of degenerative and atrophic changes in the nuclei of hair cells in the cochleae. Carnosine compensated the deficiency of tissue antioxidant systems and suppressed generation of lipid peroxidation products in tissues of the membranous cochlea and auditory cortex of the temporal lobes. Carnosine holds much promise as a nonspecific otoprotector.

Animals↗
PubMed2003

[Efficacy of 4'-thio-5-ethyl-2'-deoxyuridine (TEDU) and its derivatives in experimental infection in mice caused by herpes simplex virus].

It was demonstrated that several 5'-phosphonates of 4'-thio-5-ethyl-2'-deoxyuridine possessed antiviral activity in vitro and in the murine model of herpes simplex virus type 1 infection. It was shown that the derivatives after intraabdominal administration penetrated effectively into the brain tissue. The agents provided statistically significant increase of the average life span, lower virus titre in the brain and lower lethality when compared to the control group of the animals. It is emphasized that the derivatives were less toxic than the original compound.

Animals↗
PubMed2000

[A photoreactive analogue of 2'3'-dideoxyuridine 5'-triphosphate: preparation and use for photoaffinity modification of human replication protein A].

A new reagent for photoaffinity modification of biopolymers, 5-[E-N-(2-nitro-5-azidobenzoyl)-3-amino-1-propen-1-yl]-2',3'-dideoxyuridine 5'-triphosphate (NAB-ddUTP), was synthesized. Like a similar derivative of 2'-deoxyuridine 5'-triphosphate (NAB-dUTP), it was shown to be able to effectively substitute for dTTP in the synthesis of DNA catalyzed by eukaryotic DNA polymerase beta and to terminate DNA synthesis. A 5'-32P-labeled primer with a photoreactive group at the 3'-terminus was derived from NAB-ddUTP and used for photoaffinity labeling of the human replication protein A (RPA). The covalent attachment of RPA p32 and p70 subunits to the labeled primers was demonstrated. NAB-ddUTP is a promising tool for studying the interaction of proteins of the replicative complex with NA in cellular extracts and living cells during the termination of DNA synthesis.

DNA-Binding Proteins↗
PubMed1998

[Practical games as one of the forms for optimizing the academic process in physician postgraduate training].

Described in the article is one of the forms of optimization of the instructional process in the postgraduation physician training--"business-like games". Highly skilled, competent position of the teacher who conducts a business-like game secures an active participation in learning of students, helps in opening the mind, broadening the outlook on the problem under consideration, gives much incentive to further independent work on the discussed issues.

Diagnosis, Differential↗
PubMed1997

Opening of cardiac sarcolemmal KATP channels by dinitrophenol separate from metabolic inhibition.

Opening of ATP-sensitive K+ (KATP) channels by the uncoupler of oxidative phosphorylation, 2,4 dinitrophenol (DNP), has been assumed to be secondary to metabolic inhibition and reduced intracellular ATP levels. Herein, we present data which show that DNP (200 microM) can induce opening of cardiac KATP channels, under whole-cell and inside-out conditions, despite millimolar concentrations of ATP (1-2. 5 mm). DNP-induced currents had a single channel conductance (71 pS), inward rectification, reversal potential, and intraburst kinetic properties (open time constant, tauopen: 4.8 msec; fast closed time constant, tauclosed(f): 0.33 msec) characteristic of KATP channels suggesting that DNP did not affect the pore region of the channel, but may have altered the functional coupling of the ATP-dependent channel gating. A DNP analogue, with the pH-titrable hydroxyl replaced by a methyl group, could not open KATP channels. The pH-dependence of the effect of DNP on channel opening under whole-cell, cell-attached, and inside-out conditions suggested that transfer of protonated DNP across the sarcolemma is essential for activation of KATP channels in the presence of ATP. We conclude that the use of DNP for metabolic stress-induced KATP channel opening should be reevaluated.

Adenosine Triphosphate↗
PubMed1997

Use of the MTT assay in adult ventricular cardiomyocytes to assess viability: effects of adenosine and potassium on cellular survival.

This study used the colorimetric MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide)] assay to assess cell viability in isolated quiescent adult guinea-pig ventricular myocytes exposed to different insults or cardioprotective conditions, including adenosine and hyperkalemic-cardioplegia. Optical density (OD), reflecting intracellular reduction of MTT into formazan pigment formation, was a function of the number of viable cells (coefficient of linear correlation approximately 0.99), with MTT reduction preferentially carried out by rod-shaped cardiomyocytes (absorbance at 1.009 +/- 0.013 and 0.006 +/- 0.001 OD units for populations containing 50 and 0% of rod-shaped cells). Following prolonged mechanical (pressure of 1 lb/min for 40 min), chemical (10% DMSO or ethanol) or hypoxic injury (N2-saturated solution), the MTT reductase activity reflected reduction in the number of viable cells by 87%, >50%, and 77%, respectively. In cardiomyocytes exposed to a 40 min hypoxia (with CO2), the MTT reductase activity was 0.056 +/- 0.009 in the absence, and 0.074 +/- 0.008 OD units in the presence of adenosine (1 mM), i.e. adenosine reduced the number of non-viable cells. Also, the MTT assay revealed that the effect of potassium-containing solutions (16 and 32 mM K+) on cellular viability may depend on the extent of insult imposed on cardiomyocytes; i.e. a approximately 24% and 49% increase under mild hypoxia (0.03% CO2), or an 18% decrease in cell viability under severe hypoxia (N2) in pre-injured cells. Thus, the MTT assay used to assess viability of isolated adult cardiomyocytes revealed a direct cytoprotective effect of adenosine and hyperkalemic-cardioplegia by promoting cell survival under certain conditions in vitro.

Adenosine↗
PubMed1996

A disrupter of actin microfilaments impairs sulfonylurea-inhibitory gating of cardiac KATP channels.

The efficacy with which sulfonylurea drugs inhibit cardiac ATP-sensitive K+ (KATP) channels is reduced during metabolic compromise and cellular contracture. Disruption of the actin microfilament network, which occurs under similar conditions, reduces the sensitivity of the channel toward intracellular ATP. To investigate whether a disrupter of actin microfilaments could also affect the responsiveness of the KATP channel to sulfonylurea drugs, single-channel currents were measured in the inside-out configuration of excised patches from guinea pig ventricular myocytes. Treatment of the internal side of patches with deoxyribonuclease (DNase) I (100 micrograms/ml), which forms complexes with G actin and prevents actin filament formation, antagonized sulfonylurea-induced inhibition of KATP channels that was coupled with a loss of sensitivity to ATP. The apparent dissociation constant and Hill coefficient for the inhibitory effect of glyburide, a prototype sulfonylurea, on KATP-channel opening were, respectively, 0.13 microM and 0.95 before and 2.7 microM and 0.98 after DNase treatment. DNase did not alter intraburst kinetic properties of the channel. When DNase was denatured or coincubated with purified actin (200 micrograms/ml), it no longer decreased glyburide-induced channel inhibition. This suggests that sulfonylurea-inhibitory gating of cardiac KATP channels may also be regulated through a mechanism involving subsarcolemmal actin microfilament networks.

Actin Cytoskeleton↗
PubMed1996

[C10-aminoderivatives of colchicine: synthesis, structure and biological activity].

Replacement of the 10-methoxy group of colchicine by amino and amino acid substituents sharply decreased its toxicity and only slightly decreased its tubulin-binding activity, and thus, gave rise to a number of weakly toxic colchicine analogs. In particular, highly active 10-(N-glycino)-10-demethoxycolchicine and 10-[N-(beta-alanino)]-10-demethoxycolchicine were prepared.

Amines↗
PubMed1993

[The permeability of the hemato-encephalic barrier for superoxide dismutase following the unilateral intracarotid hyperperfusion of the cerebral vessels].

On the model of acute blood-brain barrier injury in rats after a short-term hyperperfusion of one brain hemisphere with blood, the injection of exogenic superoxide dismutase (SOD) was accompanied by pronounced increase in the activity of SOD in the damaged brain tissue. This fact and other data of the authors on this model confirm the penetration of SOD over the microvessel endothelium into the extracellular space of the same damaged brain areas that are permeable for plasma albumin.

Animals↗
PubMed1988

[Synthesis of new terminator substrates for DNA-polymerases-- nucleoside-5'-triphosphates with modified carbohydrate residue].

Synthesis of 3'-chloro- and 3'-cyanothio-2',3'-dideoxythymidine by the reaction of 2,3'-anhydro-2'-deoxythymidine with ammonium chloride and lithium thiocyanate, respectively, has been developed. In addition, 3'-methanesulphonylamido- and 3'-sulphonylamido-2',3'-dideoxythymidines were synthesized starting from 3'-amino-2',3'-dideoxythymidine. All these compounds along with 2',3'-anhydroriboadenosine,2',3'-anhydrolyxoadenosine, 2',3'-O-isopropylidenecytidine, and 2,3'-anhydro-2'-deoxythymidine were transformed into 5'-triphosphates by treatment with phosphoryl tris-1,2,4-triazolide and then with bis(tri-n-butylammonium)pyrophosphate. All 5'-triphosphates of nucleoside analogues were tested as termination substrates in cell-free systems with various DNA polymerases.

Animals↗
PubMed1987

[Analogs of deoxyribonucleoside-5'-triphosphates modified in the base and sugar moieties: substrate properties in DNA biosynthesis in cell-free systems].

Incorporation of 2'-deoxyribonucleotide 5'-triphosphate derivatives, chemically modified both in the base and at 3'-position, into DNA by four different DNA polymerases was investigated. It is shown that 3'-azido- and 3'-amino-2',3'-dideoxy-(E)-5-(2-bromovinyl)-uridine 5'-triphosphates effectively terminate DNA synthesis catalyzed by E. coli DNA polymerase I, rat liver DNA polymerase beta, and AMV reverse transcriptase. Calf thymus DNA polymerase alpha incorporates only the 3'-amino derivative. DNA polymerases I and beta catalyse DNA synthesis in the presence of beta-D-(2'-deoxyribofuranosyl)-1-benzimidazol 5'-triphosphate, inserting the corresponding monophosphate in place of -dGTP, whereas 3'-substituted analogues of this compound were inactive in the reactions.

Cell-Free System↗