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V V Liakhovich

Publications and source records attributed to V V Liakhovich.

At least 19 recordsLinked to original sources
PubMed2004

[Restriction analysis of N-acetyltransferase 2 gene in Caucasian population of West Siberia].

Restriction analysis of the NAT2 gene was carried out in inhabitants of Novosibirsk. Polymorphism of this gene for nine known point mutations was studied in a sample of Novosibirsk residents consisting of 109 healthy Caucasians. The frequencies of these mutations did not significantly differ from the frequencies reported for Caucasian populations of other countries. In 79 patients with lung cancer, a region of the NAT2 gene that includes 29.7% of the coding sequence was analyzed for the new mutations by the RFLP analysis. No new mutations were found in this group.

Arylamine N-Acetyltransferase↗
PubMed2002

[Polymorphic genes of xenobiotic-metabolizing enzymes associated with bronchial asthma in genetically predisposed children].

The frequencies of the CYP1A1 valine allele, homozygous deletions of GSTM1 and GSTT1, and two point mutations of the NAT2 gene, (C481-->T) and S2 (G590-->A), were compared in healthy children and children having bronchial asthma. The S1 mutation was associated with resistance, and all of the other traits, with predisposition to the disease. In families of patients with diseased progenitors and in those with healthy progenitors, the estimates of the asthma risk were similar. In both groups, parameters of the trait association with the disease depended on passive smoking. At passive smoking, a trend to an overrepresentation (high odds ratio, OR) of the GSTM1 null genotype and S2 mutation of the NAT2 gene was observed, whereas the odds ratio of the GSTT1 null genotype decreased, and those of the CYP1A1 and S1 mutation of the NAT2 gene remained unchanged. The highest OR = 36.25 (P < 0.01) was characteristic of the GSTT1 null genotype in nonsmoking hereditary burdened patients. The results obtained suggest an important role of xenobiotic-metabolizing enzymes in development of bronchial asthma.

Adolescent↗
PubMed1998

[Polymorphism of CYP1A1 and CYP2D6 genes in tundra nentses and European populations of western Siberia].

Data on the first examination of the CYP1A1 and CYP2D6 genes' polymorphism in the populations of Tundra Nentsis (Yamalo-Nenetskii Autonomous District) and migrant population of Western Siberia (Novosibirsk oblast and Altaiskii krai) are presented. The frequency of the 2D6*4 mutant allele in Tundra Nentsis, characterized by a two-component Caucasoid and Mongoloid origin, was shown to be intermediate in Caucasoid and Mongoloid populations. The frequencies of the 2D6*4 and 1A1Val* mutant alleles across migrant inhabitants of Western Siberia (Caucasoid populations) were similar to that reported for the Caucasoid populations overall. Distribution of the CYP1A1 genotypes (Ile/Ile, Ile/Val*, and Val*/Val*) in Tundra Nentsis was similar to that found in Mongoloid groups. However, the frequency of the 1A1Val* allele in Tundra Nentsis was 1.5 times higher than that in the Southern Mongoloid populations (Chinese, Koreans, and Japanese).

Asian People↗
PubMed1994

[Induction of cytochromes P-4501A and 2B in various rat organs, subjected to hexachlorobenzene and aroclor 1254].

The activity and content of CYP1A1, CYP1A2, CYP2B1 and CYP2B in the liver, lung and kidney of Wistar rats treated with hexachlorobenzene (HCB), Aroclor 1254 (AR), methylcholanthrene (MC) and phenobarbital (PB) were studied. Administration of MC and AR caused an increase in the ethoxyresorufin (ER) and methoxyresorufin (MR)-O-dealkylase activities in all organs. The effect of HCB on lung and kidney monooxygenases was considerably lower. The penthoxyresorufin (PR)-O-dealkylase activity in extrahepatic organs was at the same level for all treatments used in this study. Western blot analysis using monoclonal antibodies against CYP1A and CYP2B also revealed a tissue-specific expression of these proteins during different inductions. Whereas in the liver during MC, AR and HCB inductions one revealed immunologically identical CYP1A1 and CYP1A2, in MC lung only CYP1A1 was observed. In the lung of AR and HCB microsomes both CYP1A1 and CYP1A2 were found. In the kidney after treatment with AR or HCB only CYP1A1 was induced. These findings suggest that inducers of mixed type cause coordinated synthesis of CYP1A1 and CYP1A2 in the lung unobserved during MC induction. After treatment of rats with PB both CYP2B1 and CYP2B2 were observed in the liver, while only the former was found in the lung and kidney. HCB treatment did not significantly affect the induction picture. In the liver and lung of AR-treated rats, besides CYP2B1 and CYP2B2, one more P-450 was revealed whose nature is under discussion now. The data obtained thus suggest that induction of different P-450s is not only tissue-specific but also depends on the inducer type.

Animals↗
PubMed1994

[Induction of cytochrome P-450 1A1 in rat liver by ultrasound].

Rat liver monooxygenase activities, such as androstenedione (AD)-hydroxylase, pentoxyresorufin (PR)- and ethoxyresorufin (ER)-O-deethylases have been studied under contact application of ultrasound (US). In the livers of US-treated rats the AD-hydroxylase activity did not differ from the control, thus suggesting that CYP2A1, CYP2B1, CYP2C11, CYP3A1 were not induced. The rate of ER-deethylation increased from 100 in control up to 300 pmol/min/mg in US-treated rats. Western blot analysis revealed also the CYP1A1 induction in US-treated rats which was absent in untreated animals. The mRNA level for CYP1A1 in the livers of US-treated rats increased from 0.5 up to 6.0 fmol mRNA/total RNA but did not change for CYP1A2. The results obtained provide evidence for the nonchemical induction of CYP4501A1 which is known to be induced by polycyclic aromatic compounds as well as by some other compounds.

Animals↗
PubMed1992

[The effect of tetrahydrofuran on the microsomal monooxygenase system in vitro and in vivo].

The effects of tetrahydrofuran (THF) on rat liver microsomes in vitro and in vivo were opposite. In vitro THF inhibited the p-nitrophenol (PNP) hydroxylase activity of microsomes from control rats and from rats treated with PB, acetone, and isoniazide--by 50, 20, 60, and 80%, respectively. THF inhibited dimethylnitrosamine (NDMA) demethylation in control and induced microsomes in a lesser degree. THF increased the total cytochrome P-450 content as well as the contents of cytochromes P-450IIE1 and P-450IIB1/B2. The activities of PNP-hydroxylation and NDMA-demethylation increased also, whereas the PR-dealkylation activity was unchanged. An increase in the THF dose caused inhibition of the rat liver microsomal monooxygenase system.

Acetone↗
PubMed1992

[Activity of cytochromes P-450p and P-450h in liver microsomes and blood corticosteroid levels in experimental animals under the action of physical factors].

In experiments on male Wistar rats it has been found that physical factors applied in medicine (laser radiation of low intensity with wave length 0.89 microns, microwaves of centimeter range of 2450 MHz, and ultrasound of low intensity 880 KHz) changed catalytic activity of liver microsomal and rostenedione 16 alpha- and 6 beta-hydroxylating cytochromes P-450h and P-450p and blood corticosteroids level. Activities of these two steroid-metabolizing cytochromes decreased under ultrasonic skin application on liver region and increased under microwave and laser action. Contents of physiologically inactive form of corticosterone were not changed by the physical factors action while level of active hormone was increased under ultrasonic and microwave action. These findings suggest association of the activity of liver steroid-metabolizing cytochromes P-450 and level of physiologically active form of corticosterone in blood under physical factors skin application on liver region.

Adrenal Cortex Hormones↗
PubMed1992

[The effect of pyridine and pyridine-N-oxide on the monooxygenase system of rat liver microsomes].

Effects of pyridine and pyridine-N-oxide on the monooxygenase system of rat liver microsomes have been studied. Pyridine (200 mg/kg) increased total cytochrome P-450 content and activated metabolism of some specific substrates 24 hours after injection. There was an increase in the degree of p-nitrophenol and chlorzoxazone hydroxylation due to increasing ethanol-induced cytochrome P-450IIE1 content. Pyridine was also able to induce cytochrome P-450IIB1 in rat microsomes; this reaction was accompanied by acceleration of 7-pentoxyresorufin 0-dealkylation. Cytochrome P-450IA1 appearance in liver microsomes was associated with increasing content of cytochrome P-450IA2. Dealkylation rates for specific substrates (7-ethoxyresorufin and 7-methoxyresorufin) were also increased. Similar to pyridine, pyridine-7-oxide induced cytochromes P-450IIE1, P-450IIB1/B2, and P-450IA1/A2, resulting in activation of specific substrate metabolism. Hence, pyridine and its derivative pyridine-N-oxide can be regarded as effective inducers of cytochrome P-450.

Animals↗
PubMed1990

[Functional characteristics of cytochromes P-4501A1 and P-4501A2 in rodent liver].

Antibodies to mouse liver cytochrome P3-450 (anti-P3-450) and antibodies to rat liver cytochrome P-450d (anti-P-450d-c) inhibit the 0-deethylation of 7-ethoxyresorufin (ER) in liver microsomes of benz(a)pyrene-induced (BP) mice but do not inhibit the 0-deethylase activity in liver microsomes of BP-induced rats. Anti-P3-450 and anti-P-450c inhibit BP-hydroxylation in BP-induced mouse liver microsomes by 20%, but they do not inhibit this reaction at all in BP-induced rat liver microsomes. In a reconstituted monooxygenase system isolated cytochrome P3-450 metabolized 7-ER and BP. In contrast, its homologue, cytochrome P-450d, did not metabolize these substrates. The fraction containing cytochrome P1-450 metabolized 7-ER at a low rate and BP at a rate of 3.6 nmol product/min/nmol cytochrome. Western blot analysis with anti-P-450c + d revealed two bands in SDS-PAGE gels containing BP-induced mouse liver microsomes. The interaction of mouse liver BP-microsomes with anti-P3-450 and anti-P-450d-c was accompanied by the appearance of a single band (cytochrome P3-450).

Animals↗
PubMed1990

[Diazepam metabolism by multiple forms of cytochrome P-450 in rat liver microsomes].

The synthesis of pharmacologically active diazepam metabolites (oxazepam, 4-hydroxydiazepam, N-demethyldiazepam) in liver microsomes of intact and phenobarbital-, 3-methylcholanthrene- and dexamethasone-induced male and female Wistar rats as well as in a reconstituted system with isolated forms of cytochrome P-450 (P-450a, P-450b, P-450c, P-450d and P-450k according to the Ryan nomenclature) was studied. Marked sex-dependent differences in the rates of diazepam metabolism in liver microsomes of intact and induced animals were revealed. The changes in the spectrum of diazepam metabolites in liver microsomes of induced rats (as compared to control animals) were revealed. In a reconstituted system only phenobarbital-induced cytochromes P-450b and P-450k were found to be active participants of diazepam N-demethylation; none of the isoenzymes tested were shown to be involved in diazepam hydroxylation.

Animals↗
PubMed1990

[Induction of cytochrome P-450 forms by prolonged administration of nifedipine].

In experiments on male Wistar rats it has been found that nifedipine applied in a dose of 10 mg/kg body weight i.p. daily for 20 days did not significantly increase the total amount of cytochrome P-450 but markedly increased the 7 alpha-, 16 beta- and 6 beta-hydroxylation of androstenedione in liver microsomes, suggesting the induction of cytochromes P-450a, P-450b and P-450p respectively. The induction of cytochrome P-450b was also confirmed immunochemically with polyclonal antibodies against cytochrome P-450b/e.

Androstenedione↗
PubMed1990

[Evaluation of catalytic activity of multiple forms of cytochrome P-450 in liver microsomes of Wistar rats by androstenedione metabolism].

The synthesis of androstenedione (AD) metabolites in liver microsomes of control and phenobarbital (PB)-induced male and female Wistar rats was studied. In liver microsomes of non-induced male rats the predominant formation of 16 alpha-hydroxyandrostenedione was observed, whereas in females the predominant form was the 7 alpha-metabolite. Induction of animals of both sexes with PB was accompanied by an increase in the 16 beta-hydroxylase activity. The dynamics of synthesis of other AD metabolites specifically produced by such cytochrome P-450 forms as P-450a, P-450h and P-450p was investigated. The specificity of metabolism of androstenedione by multiple forms of cytochrome P-450 is postulated.

Androstenedione↗
PubMed1990

[Comparison of the inducing effect of triphenyldioxan, bis-(dichloropyridyloxy)benzene and phenobarbital on the liver monooxygenase].

The induction by triphenyldioxane (TPD) of cytochrome P-450 in rat liver microsomes was studied. It was demonstrated that TPD injection in a single dose (10 mg/kg of body mass) is associated with a marked induction of cytochromes P-450 b/e (cytochrome PB-forms) in rat liver microsomes and a significant increase in the benzphetamine-N-demethylase activity typical of cytochrome P-450b. In other words, TPD is a potent inducer of PB-type, the inducing effect being attained by an injection of a single dose of TPD which is by one order of magnitude less than that of phenobarbital. It can be assumed that this compound shows a high affinity for the hypothetical receptor responsible for cytochrome P-450b synthesis. It was shown also that TPD does not induce the monooxygenase system of mouse liver, whereas 1,4-bis[2-(dichloropyridyloxy)]benzene (DPB) is a potent inducer of PB-type in mice, being fairly ineffective in rats. Hence, the species-specific effect of TPD and DPB appears to be opposite.

Animals↗