PubMed Health⌕ Search

Biomedical subjects

Iu M Ostrovskiĭ

Publications and source records attributed to Iu M Ostrovskiĭ.

At least 19 recordsLinked to original sources
PubMed1989

[Formation of taurine and amino acid pools in rat tissues upon stimulation of NAD synthesis].

A single intraperitoneal injection of nicotinamide (500 mg/kg) to mongrel albino rats causes a 6-hour increase in the 2-oxoglutarate level and the free NAD+/NADH ratio in liver mitochondria. The levels of taurine and taurocholates as well the activity of cysteine oxidase in liver tissues remains thereby unchanged, whereas the cysteine transaminase activity diminishes. In the heart and brain of experimental animals the activity of both enzymes is decreased. In the liver, blood plasma and heart of experimental animals, the Ala and Ser levels are low, whereas the taurine content is elevated both in blood plasma and brain. Nicotinamide administration eliminates positive correlations between the levels of taurine, its precursors and metabolically bound amino acids. In the liver the negative correlations between the activities of cysteine oxidase and cysteine transaminase observed in the control group disappear in the experimental group. Apparently, one of regulatory mechanisms of the taurine pool formation in the liver is the ratio of activities of the both enzymes as well as their competition at the substrate level. This emphasizes the importance of the transamination reactions in the metabolism of sulphur-containing amino acids.

Amino Acids↗
PubMed1988

[The action of nicotinamide on the adenine nucleotide system as well as on mitochondrial oxidation and phosphorylation processes in the liver of db/db strain mice].

Both levels of total adenine nucleotides, ATP, AMP, ATP/ADP ratio and phosphate potential of cell and cytosol and the intensity of mitochondrial oxidation (fatty acid beta-oxidation in particular) and phosphorylation are elevated in the liver of db/db mice as compared with control. Presumably these alterations corresponding to the total activation of metabolic processes in db/db mice are mediated by hyperinsulinemia. Nicotinamide treatment (2.5 mg/100 g body weight, 14 days, i.m.) elicits further increase of ATP and total adenine nucleotide levels, cytosolic phosphate potential and activation of mitochondrial oxidation and phosphorylation. The findings obtained can be used for explanation of nicotinamide inhibition of gluconeogenesis, diacylglycerol and phosphoacylglycerol biosynthesis in the liver of db/db mice.

Adenine Nucleotides↗
PubMed1988

[Aldehyde dehydrogenase activity in the barrier brain structures].

The histochemical method was used to study the aldehyde dehydrogenase (EC 1.2.1.3.; ALDH) activity in capillaries and glial structures of different regions in the rat central nervous system (CNS). The occurrence of three metabolic barriers for aldehydes on systemic level in the CNS has been shown. They are: the barrier between blood and the nervous tissue (represented by capillary endothelium and surrounding astrocytes ALDH), that between blood and cerebrospinal fluid (ALDH in ependymocytes of vascular plexus), and that between cerebrospinal fluid and nervous tissue (ALDH of ependymocytes covering brain cavities). On the single microregions level a similar barrier is between interstitial fluid and neurons (ALDH of satellite oligodendrocytes).

Aldehyde Dehydrogenase↗
PubMed1988

[Effect of phosphopantothenate on the biosynthesis of cholesterol and its esters from various precursors in the liver of db/db mice].

It was found that in the livers of db/db mice with hyperinsulinemia, obesity and non-insulin-dependent diabetes the rates of cholesterol biosynthesis from pyruvate and, to a lesser extent, from acetate and mevalonate as well as of cholesterol ester biosynthesis from pyruvate (but not from acetate and mevalonate) are increased. Presumably, the observed changes are mediated by structural alterations in the CoA reserves, i.e., increase of free CoA to short-chain acyl-CoA and free CoA to long-chain fatty acyl-CoA indices, and of the ratio between enzymatic activities of generation and utilization of NADPH. Treatment of db/db mice with phosphopantothenate, besides eliciting changes in the CoA reserves structure towards normalization and inhibition of NADP-dependent dehydrogenases and pyruvate and 2-oxoglutarate dehydrogenase complexes, causes the diminution of cholesterol and its ester levels in the liver in the absence of any conspicuous changes in the rates of their biosynthesis from pyruvate.

Acetates↗
PubMed1987

[Endogenous blood ethanol in alcoholic patients and healthy subjects with and without a family history of alcoholism].

Levels of endogenous ethanol were studied in healthy males, 12-13-year-old boys (sons of alcoholics and normal fathers) and alcoholic patients (after discontinuation of all drugs). The results showed no significant differences between the groups. On the other hand endogenous ethanol concentrations were higher than normal in oligophrenic boys irrespective of whether their fathers were alcoholics or healthy subjects. In the abstinence period endogenic ethanol concentrations were the minimal in patients with delirium tremens and a severe abstinence syndrome, the dynamics of this parameter in the process of treatment being dependent on the severity of the abstinence syndrome and on the nature of treatment.

Adolescent↗
PubMed1987

[Characteristics of intracellular metabolism of carbohydrates and amino acids in animals with thiamine deficiency].

Vitamin B1 deficiency in mongrel albino rats induced by oxythiamine is concomitant with an increase in the ratio of free forms of NAD+/NADH, NADP+/NADPH in liver mitochondria. This is accompanied with a rise in steady-state concentrations of isocitrate, 2-oxoglutarate and with a decrease of malate in liver tissue, which testifies to the prominent regulatory role of the 2-oxoglutarate dehydrogenase complex in the intracellular metabolism under vitamin B1 deficiency. Moderate physical load causes a 10-fold increase in the steady-state concentration of pyruvate and lactate in the blood of thiamine-deficient animals, which seems to be due to the stimulation of glycolysis in the maintenance of energy homeostasis. The observed increase in the excretion of pyruvate, lactate, 2-oxoglutarate (30-fold against control) and pentose phosphates (3-fold) with urine, depending on the degree of vitamin B1 deficiency, points to one of essential mechanisms of cell metabolism stabilization under the given pathological condition.

Acetone↗
PubMed1986

[Characteristics of thiamine thiazolone diphosphate-induced inhibition of a pyruvate dehydrogenase complex in vitro and in intact mitochondria].

Thiamine thiazolone diphosphate (TTPP) was capable of penetrating through the mitochondrial membrane and of inhibiting the pyruvate dehydrogenase complex (PDC) in intact mitochondria. TTPP depressed the activity of mammalian PDC in a mixed manner (Ki = 5.10(-8) M) and yeast pyruvate decarboxylase (Ki = 5.10(-6) M) via a competitive mechanism with respect to thiamine diphosphate. It was shown that decarboxylation of pyruvate in intact and disrupted mitochondria of rat liver and brain is less inhibited by TTPP than the overall activity of PDC determined by the formation of acetyl-CoA. It was assumed that TTPP as a transition state analog participates only in oxidative reactions (but not in simple decarboxylation of pyruvate).

Adrenal Cortex↗
PubMed1985

[Characteristics of carbohydrate metabolism in the rat liver in thiamine deficiency].

Thiamine deficiency in rats induced by oxythiamine is accompanied by an increase in the free NADP+/NADPH ratio in liver tissue, which results in multifold stimulation of the metabolite flux in the oxidation branch of the pentose cycle. The increase in the intracellular concentrations of isocitrate and alpha-ketoglutarate with a simultaneous decrease of malate in the liver of vitamin-deficient rats points to the inhibition of alpha-ketoglutarate dehydrogenase responsible for the anomalous metabolism under conditions of thiamine deficiency. The decrease of the functional activity of the tricarboxylic acid cycle is concomitant with the activation of conversions in the oxidation branch of the pentose cycle, glucuronate and glycolytic pathways of carbohydrate metabolism, which is directed at eliminating the energy deficiency in rats with B1-hypovitaminosis.

Animals↗
PubMed1979

[Tumor and body interrelationships in 14C-thiamine utilization].

Variations in the content of 14C-thiamine, thiamine-dependent enzyme transketolase (TK), and thiamine diphosphate (TDP) in mouse tissues were studied during Ehrlich's ascites tumour growth. The concentration of TDP in the liver of tumour-bearing animals continuously drops during 10 days after inoculation, TDP level in the tumour itself decreases more abruptly by the terminal period of tumour growth (the 10th day). At the same time the tumour demonstrates sharp deficiency of the coenzyme and redundance of apoenzymatic forms of TK. The growing deficiency of thiamine in the tumour favours greater tension of thiamine metabolism and appearance of competitive tumour-host interrelationships that are most pronounced in the presence of hypovitaminosis.

Animals↗
PubMed1978

[Kinetic characteristics of thiamine diphosphate biosynthesis by thiamine pyrophosphokinase from rat liver].

The kinetic analysis of bisubstrate enzymatic reaction catalysed by electrophoretically homogenous thiamine pyrophosphokinase (EC 2.7.6.2), isolated from rat liver has been carried out. Kinetic studies of the initial rates in the absence of the products and inhibition by the reaction products as well as the data from the equilibrium dialysis suggest that the reaction proceeds through the formation of a ternary enzyme-substrate complex. The combination with substrates and release of the products appears to be highly ordered. A possible scheme of the reaction mechanism is discussed.

Animals↗
PubMed1978

[Free amino acid concentration in the tissues of rats with different forms of thiamine deficiency].

The levels of free amino acids in rat tissues under thiamine deficiency induced by antivitamin (oxithiamine) and under thiamine-deficient diet were studied. Changes in the amino acid pool at these two forms of vitamin B1 deficiency were revealed. The most typical change consists in extensive accumulation of alanine and glutamate with a simultaneous decrease in the amount of many other essential and non-essential amino acids. The disturbances in the amino acid pool under thiamine deficiency may be probably regarded as resulting from inhibition of alpha-keto acid dehydrogenase activities.

Amino Acids↗
PubMed1977

[Biosynthesis of mitochondrial protein in rat liver under conditions of vitamin B 1 deficiency following oxythiamine injection].

The incorporation of labelled precursors into mitochondrial proteins of liver under different duration of oxythiamine (antivitamin B1) effect was studied in the whole organism and in a cell-free system. After 24 hrs following the injection, oxythiamine at a dose of 400 mg/kg of body weight increases the mitochondrial protein synthesis in vivo without changing the protein-synthesizing capacity of isolated mitochondria. After 72 hrs following the injection of the same dose of preparation, a sharp increase in the rate of protein label incorporation into the mitochondria was observed. The protein synthesis in mitochondria in the whole body studies also showed an increase. It is assumed that oxythiamine enhances the inductive synthesis of mitochondrial thiamine phosphate-dependent enzymes or activates the syntheses of other enzymic systems, capable of increasing the utilization of alpha-keto acids accumulated under conditions of thiamine deficiency.

Animals↗
PubMed1977

[Possible mechanism of action of oxythiamine on nucleic acid metabolism].

Hydoxythiamine injections (400 mg/kg for 72 hours) resulted in the inhibition of transketolase activity and of 14C-orotic acid incorporation into RNA in rat liver tissue. At the same time, the decrease of RNA and phosphoribosylpyrophosphate levels has been observed, which suggests a regulation effect (via pentospohosphates) of hydroxythiamine on nucleotide and nucleic acid metabolism.

Animals↗