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Biomedical subjects

G A Belitskiĭ

Publications and source records attributed to G A Belitskiĭ.

At least 19 recordsLinked to original sources
PubMed2006

[Carcinogenic components of smokeless tobacco and tobacco-free cigarettes].

The investigation deals with an assessment of carcinogenicity and mutagenicity of samples of smokeless tobacco now on the Russian market as well as ash from alternative cigarettes made of aromatic herbs. Our data showed that the levels of polycyclic aromatic hydrocarbons, volatile and tobacco-specific N-nitrosoamines complied with the standards in the producer-countries. Smokeless tobacco extracts failed to show (Ames) any mutagenic effects such as the "read-out frame shift" or "base-pair replacement" patterns. No tobacco-specific N-nitrosoamines were identified in herbal cigarettes. However, polycyclic aromatic hydrocarbons and volatile N-nitrosoamines content appeared to be identical to that of tobacco. Herbal cigarette smoke extracts mutagenicity induced by side-effects of carcinogenic substances was of similar magnitude as well.

Carcinogens↗
PubMed2004

[Mammalian carcinogen-induced warts tumor in Drosophilidae: a test sensitive to the blastomogenic action of chemical compounds].

A basically new system has been developed to screen carcinogens in Drosophilidae, which is based on somatic mutagenesis and recombination. The system may induce tumors in Drosophilidae, which are recorded in adult insects. The test uses recessive mutation in the suppressor gene of growth of warts (wts) tumors. The new system is sensitive to a wide spectrum of mutagenic carcinogens that are naturally encountered. The sensitivity of the system to polycyclic aromatic hydrocarbons and aromatic amides is higher than that of classical tests. Dominant p53 gene mutation that ceases mutagen-induced apoptosis has been shown to increase the incidence of wts tumors by many times. The magnitude of the effect depends on the rate of mutant p53 expression. The increasing effect of p53 mutation extends to both somatic recombination and point mutations and deletions at the wts locus.

Animals↗
PubMed2002

[The effect of transposon P(GUS . p53.259H)on the frequency of tumor clones in Drosophila melanogaster wtsp2/+ heterozygotes].

We showed that transposon P(GUS.p53.259H), mapped to chromosome 3 and carrying a dominant mutation p53(259)H.GUS, has a positive effect on the frequency of spontaneous and carcinogen-induced tumor mosaic clones warts- in Drosopila melanogaster heterozygotes for the tumor suppressor gene warts located in the same chromosome. The transposon effect could be explained either by the arrest of apoptosis in the cells expressing mutant p53(259)H.GUS gene and containing carcinogen-induced pre-mutations, and/or by genetic instability introduced into chromosome 3 by the P(GUS.p53.259H) transposon itself. The effect of the P(GUS.p53.259H) appeared to be carcinogen-specific. It substantially increased the frequency of tumors induced by supermutagenic platinum complex, oxoplatin, and did not increase the frequencies of tumors induced by polycyclic aromatic hydrocarbons, benzo(alpha)pyrene and pyrene. In the spectrum of mutations induced by all carcinogens tested, somatic recombination events prevailed over somatic mutations. Hence, carcinogen-specificity of the P(GUS.p53.259H) effect cannot be explained by preferential induction of somatic mutations or somatic recombination by one of the carcinogens. Organ-specificity of the increased frequency of mosaic warts- clones induced by P(GUS.p53.259H) was established.

Animals↗
PubMed1999

[Absence of mutagenic and carcinogenic properties in Mildronate].

Mutagenic and carcinogenic properties of mildronate (3-[2.2.2.-trimethyl hydrazonium]-propionate) have been studied for its marked immuno-stimulating and anti-ischemic action. When dosage up to 1,000 mg/dish was used no reversal of base-pair substitution or frame shift in S.typhimurium was observed. In drosophila females treated with mildronate, mosaic patches were, on the average, as frequent as in control. Although chronic treatment of female mice B6D2F1, C3H and SHR with mildronate was not followed by any change in tumor incidence, mammary gland adenocarcinoma development was slightly inhibited in mice C3H and SHR. The latter effect was in correlation with the antigonadotropic one of the drug and was not determined by its estrogenous properties. This pointed to the absence of mutagenic and carcinogenic properties which was confirmed in two short-term and one chronic experiments on mice of the three lines.

Adenocarcinoma↗
PubMed1991

[Benzo(a)pyrene pretreatment of Drosophila simulans mutant strain results in the induction of aberrant isoform of cytochrome P-450 with increased capacity to metabolize benzo(a)pyrene].

The basal level of benzo(a)pyrene monooxygenase, epoxide hydrolase and glutathione S-transferase activity as well as the content of cytochrome P-450 were found the same in both compared benzo(a)pyrene (BP) sensitive D. simulans strain 364yv and BP-resistant wild one (Turku). Phenobarbital pretreatment resulted in the same increase level of these enzyme activities in both strains. BP-pretreatment of 364yv flies decreased the amount of the cytochrome P-450 but raised up the turnover of BP per molecule of cytochrome P-450. SDS-polyacrylamide gel electrophoresis of the microsomal proteins from BP-pretreated 364yv flies (but not from Turku) showed an increased hemoprotein content in the 56000 band. The relationship between BP-sensitivity of the strain 364yv and BP-induced aberrant isoform of the cytochrome P-450 has been discussed.

Animals↗
PubMed1991

[The specificity of the genotoxic action of carcinogenic aromatic compounds on Drosophila mus mutants].

Hypersensitivity to the toxic effect of benzo(a)pyrene (B(a)P) was determined in homozygous larvae of two D. melanogaster mus strains (mus 208B2 and mus210). The two others (mus205B1 and mus208B1) were found to be less sensitive and the parent strain was resistant. The lack of correlation between the sensitivity in larvae and the activity of aryl hydrocarbon hydroxylase in S15 fractions from adult flies whole body homogenates of the same strains was demonstrated. The hypertoxic effect of B(a)P and 2-acethylaminofluorene in strain mus210 seems to be rather specific because noncarcinogenic pyrene, benzo(e)pyrene and fluorene did not affect the survival of this most sensitive strain. Perspectives of the strain mus210 use for the environmental genotoxic pollutants screening were discussed.

Animals↗
PubMed1991

[A mutant strain of Drosophila simulans sensitive to the toxic and mutagenic action of benz(a)pyrene].

A 364 yv strain sensitive to the toxic effect of benzo(a)pyrene (BP) was identified among 49 mutant strains of Drosophila simulans. Heterozygotes female 364 x male Turku obtained by crossing 364 yv species with those of wild BP-resistant Turku strain were more sensitive than female Turku x male 364 heterozygotes to both toxic and mutagenic effects of the carcinogen in the test of induction of somatic mosaicism with the yellow marker. Non-carcinogenic pyrene appeared weekly toxic and non-mutagenic. Possible mechanisms of 364 yv strain sensitivity to BP as well as vistas in application of the strain for monitoring genotoxic environmental pollution are discussed.

Animals↗
PubMed1990

[Direct-action mutagens in exhausts of vehicles with diesel engines].

The genotoxic activity of exhausts from one-shaft gas-turbine GTE-5 engine (30 kW) and a standard D-54A diesel (40 kW) have been studied. Thus, the extracts of soot from GTE-5 and D-54A induced reversions in Salmonella typhimurium both with and without metabolic activation: furthermore, extracts of soot from GTE-5 demonstrated a higher mutagenic activity. The direct mutagenic effect of the exhausts depended neither on the presence of BP nor on the other polycyclic aromatic hydrocarbons (PAHs). Most probably, it was connected with the presence of nitro-PAHs. The need for studying the PAH content in vehicle engines' exhausts and for taking into account their effect in the control and standardization is established.

Benzopyrenes↗
PubMed1990

[The mutagenic activity of coal tar].

Genotoxicity of tar samples collected at the Kemerovo and Altai by-product coke plants has been studied, the contribution of benz(a)pyrene (BP) into the total mutagenic activity of extracts being estimated. Both direct and indirect mutagenicity of the samples is determined in the Ames test. A direct mutagenic effect of coal tar may be attributed neither to the BP action nor to other polycyclic aromatic hydrocarbons. The onset of the His revertant induction in Salmonella typhimurium strains Ta 100 and TA 97 treated with the coal tar activated by the S-9 mixture is observed in doses containing BP an order lower than threshold of its activity found in sole experiment. The highest mutagenic effect of the activated coal tar is observed at a dose containing the minimal active sole dose of BP (0.72-1.12 micrograms per plate).

Animals↗
PubMed1989

[Microsomal monooxygenases of the liver in mice with transplanted tumors].

Hepatoma 22a and Ehrlich's tumor growth were shown to be accompanied by decrease in cytochrome P-450 level in liver of noninbred and C3HA mice, these changes being more pronounced as compared to solid neoplasms. Benzo(a)pyrene-hydroxylase and amidopyrine-N-demethylase activity varied with tumor pattern. It was not changed in cases of hepatoma 22a but decreased in mice bearing Ehrlich's tumor, particularly, in those with the ascitic form. The inhibition analysis using metyrapone and 7,8-benzoflavone identified phenobarbital and methylcholanthrene forms of benzo(a)pyrene-hydroxylase in murine liver; isoform profile was not significantly affected by tumor. Liver microsomal monooxygenases of tumor-bearing mice retained inducibility by 3-methylcholanthrene.

Animals↗
PubMed1987

[Sovol as an inducer of procarcinogen activating microsomal enzymes].

The commercial mixture of polychlorinated biphenyls (Sovol) studied by biochemical and immunochemical methods was found to be an inducer of a wide range of cytochrome P-450 isoenzymes. The induced enzymes activated in the Ames test a series of procarcinogens differing both in structure and in target organs: benz(a)pyrene, 3-methylcholanthrene, nitrosomorpholine, dimethylnitrosamine, aflatoxin B1, orthoaminoazotoluene, 2-acetylaminofluorene, cyclophosphamide and benzidine. According to the parameters the studied Sovol is similar to Aroclor 1254 and may be recommended to be used as an inducer of microsomal enzymes in routine tests for carcinogen screening.

Animals↗
PubMed1987

[Possibility of identifying tumor promoters by their inhibitory action on the intercellular exchange of lucifer yellow].

The effects of tumor promoter--12-0-tetradecanoylphorbol-13-acetate (TPA), mezerein, anthralin, Ca2+-ionophore A23187, butylated hydroxytoluene (BHT), DDT and phenobarbital--on cell-to-cell exchange of Lucifer Yellow were studied in cultures of SV40-transformed Djungarian hamster fibroblasts. TPA, mezerein, A23187, DDT and BHT strongly inhibited cell-to-cell exchange of Lucifer Yellow. Anthralin uncoupled cells in 3 out of 6 experiments. Phenobarbital, in contrast to other promoters, enhanced dye transfer. The effects of all the promoters tested were fully reversible. The potential use of Lucifer Yellow exchange inhibition as a test for the screening of tumor promoters is discussed.

Animals↗