Search PubMed⌕ Search

Biomedical subjects

G V Donchenko

Publications and source records attributed to G V Donchenko.

At least 91 records · Page 5Linked to original sources

[Effect of vitamin E an actinomycin D on protein and RNA synthesis in rat liver].

In vitro experiments showed that RNA synthesis intensity in the rat liver with E-hypovitaminosis decreases considerably while the level of the labelled precursors incorporation into protein does not differ from the norm. Under conditions of E-hypovitaminosis the inhibitory effect of actinomycin D on the RNA synthesis is pronounced more clearly as compared to the norm. In the case of the E-hypovitaminous rate liver chyme preincubation with alpha-tocopherol there is no inhibitory effect of actinomycin D on the protein biosynthesis.

Animals↗

[Effect of alpha-tocopherol on relations between RNA and ubiquinone biosynthesis in rat liver].

The animals were kept on the low-protein diet deprived of vitamin E. Addition of the latter to the diet fed to a noticeable increase in the intensity of the biosynthesis of total and nuclear RNA of the rat liver. alpha-Tocopherol had a clearly marked stimulant effect on the synthesis of RNA and ubiquinone as shown by in vitro experiments under 30-minute preincubation of the liver from rats with E-hypovitaminosis. Meanwhile actinomycin D was found to inhibit these processes. Under preincubation with actinomycin D or concurrent introduction of the antibiotic with alpha-tocopherol the effect of the latter does no get realized. Unlike alpha-tocopherol, ionol and other synthetic antioxidants proved ineffective. It is assumed that the stimulant effect of vitamin E on the biosynthesis of ubiquinone in the liver of rats with E-hypovitaminosis is related to the increased intensity of the RNA synthesis and differs from the antioxidant one as regards the type. It is also assumed that the action of alpha-tocopherol on the RNA synthesis is effected at the transcriptional level.

Animals↗

[Effect of vitamin E and ubiquinone-9 on activity of ubiquinone-dependent enzymic systems of rat liver mitochondria].

It is shown that the activity of succinate- and NADH-ubiquinone-reductase systems as well as the ubiquinone content in the liver mitochondria of E-hypovitaminotic rats decrease as compared to their level in the liver mitochondria of healthy animals. Under conditions of E-hypovitaminosis alpha-tocopheronolactone and ubiquinone-9 3 h after intravenous injection to rats produce a pronounced normalizing effect on the ubiquinone content and on the activity of ubiquinone-dependent enzymic systems. It is assumed that a positive effect of vitamin E and its metabolite on the activity of these enzymic systems is to a considerable extent connected with an increase in the ubiquinone content in the rat liver mitochondria.

Animals↗

[Possibility of preventing muscular dystrophy in E avitaminosis with alpha-tocopheronolactone and diludin].

The efficacy of pharmacopeial alpha-tocopheryl acetate, alpha-tocopheronolactone and the antioxidant diludin was studied as to the possibilities of preventing E-hypovitaminosis muscle dystrophy in rabbits. alpha-Tocopheronolactone action was similar to that of pharmacopeial alpha-tocopheryl acetate as regards E-vitamin activity that was manifested by an increase in the body mass, decrease in the urine creatine index and maintenance of normal ubiquinone content, as well as of succinate-ubiquinone-reductase, NADH-ubiquinone-reductase and NADH-cytochrome c-reductase activity of rabbit skeletal muscle and heart mitochondria. On the contrary , as a result of the antioxidant administration, no direct correlation was found between ubiquinone content and activity of ubiquinone-dependent enzymatic systems of mitochondria. The data obtained attest to high E-vitamin activity of alpha-tocopheronolactone. The action of the latter was disclosed to be different from that produced by the antioxidant.

Animals↗

[Determination of adenine nucleotide and inorganic phosphate contents of liver of rats with E-hypovitaminosis and administration of alpha-tocopherol and ubiquinone-9].

It is shown that in the rat liver with E-hypovitaminosis the ATP content, sum of adenine nucleotides, and the phosphate potential value ([ATP]/[ADP.]Pi) decrease, whereas the amount of ADP, AMP and Pi remains practically unchanged. 3h after intravenous administration of alpha-tocopherol of ubiquinone to rats with E-hyovitaminosis the mentioned indices normalize, which evidences for a considerable increase in the level of bioenergetic processes. The direction of the mentioned changes corresponds to changes in the ubiquinone content and activity of the respiratory chain redox enzymes. The participation of vitamin E in processes of oxidative phosphorylation may be connected with the metabolism control and ubiquinone functioning.

Adenosine Diphosphate↗

[Alpha-tocopherol and actinomycin D regulation of ubiquinone and protein biosynthesis in rat liver in E-hypovitaminosis].

In vitro experiments with the liver preparations from rats with E-hypovitaminosis revealed a more intensive incorporation of [14C]phenylalanine into ubiquinone induced by alpha-tocopherol. Actinomycin D inhibiting the DNA-dependent RNA synthesis decreases the incorporation intensity. A 30 min preincubation of the liver preparations with thesis. In case of preliminary addition of actinomycin D or its simultaneous introduction with alpha-tocopherol the latter has no stimulating effect on the intensity of [14C] phenylalanine incorporation into ubiquinone. When studying incorporation of [14C]phenylalanine into the total protein of the liver of rats with E-hypovitaminosis a tendency is revealed to an increase in the protein biosynthesis intensity in case of preincubation with alpha-tocopherol and to inhibition of the labelled precursor incorporation under conditions of preincubation with actinomycin D. The data obtained permit suggesting that the alpha-tocopherol effect on the ubiquinone biosynthesis may occur due to its effect on the RNA synthesis.

Animals↗

[Efficiency of ubiquinone and p-oxybenzoic acid in prevention of E-hypovitaminosis-induced development of muscular dystrophy].

It is shown that E-hypovitaminosis-induced muscular dystrophy in rabbits is accompanied by a sharp decrease in the body mass, an increase in the urine creatine-index, a decrease in the vitamin E and ubiquinone contents in the liver and skeletal muscle tissues. In the myocardium mitochondria a decrease in the vitamin E content and an increase in the ubiquinone content are observed. The activity of NADH-cytochrome c-, NADH-ubiquinone- and succinate-ubiquinone-reductase also varies in mitochondria of the studied tissues. In myocardium organellas a direct dependence is found between the content of ubiquinone, NADH- and succinate-ubiquinone-reductase activity and an inverse one-between its content and the activity of the NADH-cytochrome c-reductase system. It is established that p-oxybenzoic acid as well as vitamin E prevents development of muscular dystrophy and causes changes analogous in direction in the activity of the ubiquinone-dependent enzymic systems of mitochondria. Ubiquinone-9 is less efficient in preventing the development of muscular dystrophy.

Animals↗

[Effectiveness of different alpha-tocopherol derivatives in preventing experimental muscular dystrophy in chickens].

Activity of vitamin E and its derivatives--alpha-tocopheryl quinone, its short chain analogue and alpha-tocopheryl acetate also containing short chain molecule were studied during chicken experimental muscular dystrophy. alpha-Tocopheryl quinone containing short chain molecule proved to be the most active substance; similarly to vitamin E the preparation increased the erythrocyte resistance to osmotic haemolysis, distinctly increased the content of ubiquinone and decreased concentration of ubichromenol in the chicken liver tissue as compared with E-deficient animals. At the same time, the content of ubiquinone was unaltered in skeletal muscles. The data obtained suggest that vitamin E could be effectively substituted by its derivatives for prevention an treatment of muscular dystrophy.

Animals↗

[Participation of benzodiazepine receptors in the mechanism of action of nicotinamide in nerve cells].

Bicucculine being introduced to rats has induced an increase of [14C]GABA capture with synaptosomes and simultaneous decrease of GABA and NAD level in the brain. The decrease of the inhibiting effect of GABA is accompanied by the increase of specific binding of [3H]flunitrazepam with benzodiazepine receptors at the expense of the increase of binding capacity from 0.33 to 0.45 g/mol per 100 mg of protein. Under these conditions the dissociation constant remains unchanged. Such an activation of benzodiazepine receptors was observed under the lack of NAD in the organism (model of PP-hypovitaminosis). Introduction of the surplus doses of nicotinamide neutralizes the convulsant effect on benzodiazepine receptors.

Animals↗

[Effect of NAD on uptake and release of some mediators by synaptic vesicles of the rat's brain].

NAD has been studied for its effect on the uptake of serotonin, norepinephrine, dopamine and GABA by synaptic vesicles. It has been shown that norepinephrine and dopamine uptake is not altered by addition of 10(-3) M, 10(-6) M, 10(-8) M, 10(-9) M and 10(-12) M NAD concentrations to incubation medium while the serotonin uptake is increased by 29, 47, 23, 24 and 18%, respectively. 10(-3) M and 10(-6) M NAD concentrations decrease GABA uptake by 30% and 24%. The study of 10(-6) M NAD effect on serotonin release from serotonin pre-loaded vesicles demonstrated the marked elevation of the neurotransmitter release, especially during the first 4 minutes of incubation (by 40%). The similar effect on serotonin release, is observed after addition of KCl, standard depolarizing agent, to the incubation medium. In contrast to synaptic membranes, the red blood cell membranes did not activate the neurotransmitter release after addition of serotonin pre-loaded vesicles to incubation medium, which proves the specificity of synaptic vesicles--synaptic membranes interaction. The modulating NAD action at the presynaptic membrane level can also be assumed.

Animals↗

[Chromatin proteins binding vitamin E].

It was discovered that alpha-tocopherol binding with isolated chromatin is specific only when fraction of tocopherol-binding proteins from a nuclear extract with 1% triton X-100 is present. During the chromatography of chromatin incubated with [H] alpha-tocopherol on hydroxyapatite a specific binding activity was present only in fraction eluted with 2M NaCl + 5M urea. Quantitative changes in the protein content of this fraction during a hypovitaminosis are found. It is shown that vitamin E can effect the RNA polymerase activity of a nuclear matrix in the in vitro assays. It is suggested that the presence of tocopherol-binding proteins of chromatin in necessary for such an action of alpha-tocopherol.

Chromatin↗

[Study of the dynamics repair of DNA damage caused by N-methyl-N-nitrosourea during activated NAD biosynthesis in rat liver].

Dynamics of the DNA main reparative reactions was studied in rat liver tissue after N-methyl-N-nitrose urea treatment and simultaneous stimulation of NAD biosynthesis in order to evaluate the interrelationship between DNA repair and poly-ADP-ribosylation. Treatment of liver tissue with the mutagen was followed by the preparations incubation in Hanks solution within 30 min at 37 degrees. During the initial steps of restoration an increase in amount of DNA breaks proved to occur in liver tissue of the experimental animals as compared with controls; these deteriorations were decreased down to initial level to the final steps of incubation, while content of breaks in single-strand DNA remained to be high in liver tissue of control animals. The intensive rate of DNA repair in rat liver tissue containing high level of NAD correlated with an increase in nuclear endonuclease and DNA-dependent-DNA-beta-polymerase activities. At the same time, the activity of poly-ADP-ribosyl polymerase was only slightly altered during all the steps of the tissue repair studied.

Animals↗

[Interaction of the retinol-cellular-retinol-binding protein complex with nuclei of the glandular stomach mucosa cells in rooster].

Interaction of the 3H retinol-cellular retinol-binding protein complex with nuclei is shown. The uptake process is specific and saturable. Free retinol does not penetrate to a nucleus. An assumption is advanced that cellular retinol-binding protein with molecular weight 14 kDa has no specific tissues and is involved in the transport of retinol to the nucleus and to the Golgi apparatus of the glandular stomach mucosa cells.

Animals↗

[Isolation of cellular retinol-binding protein from cattle liver].

Cellular retinol-binding protein from bovine liver has been purified to homogeneity. The protein binds retinol with high affinity; the apparent dissociation constant was determined by fluorometric titration to be 2.18 x 10(-3) M. Retinol bound to the protein has an absorption spectrum (lambda max = 350 nm) and considerably differs from the spectrum of retinol absorption in ethanol (lambda max = 325 nm). The protein is a single polypeptide chain with a molecular weight of approximately 14 kDa based on information obtained by sodium dodecyl sulfate-polyacrylamide electrophoresis.

Animals↗