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Biomedical subjects

Iu V Pashin

Publications and source records attributed to Iu V Pashin.

At least 19 recordsLinked to original sources

[Mutagenic action of the dimethyl ester of terephthalic acid on murine somatic cells in vivo].

Mutagenic activity of dimethyl terephthalate (DMtP) was evaluated using the bone marrow micronucleus test in mice. Clear clastogenic effect with the highest response in 24 h after a single i.p. injection was obtained at all concentrations used (0.2-1.0 mM/kg). The time-course for the micronuclei induced by DMtP was in agreement with the literature data on fast excretion of phthalates from mammal body. The dose-response curve for DMtP-induced micronuclei was linear in form with the logarithmic component. The emergence of the latter was related to the elevation of the chemical's concentration to the level at which DMtP starts to exert toxic influence on bone marrow erythropoietic function. The comparison of the effect induced by DMtP with that of methyl nitrosourea indicated that DMtP could not be considered as a strong mutagenic compound. Susceptibility of the micronucleus test was compared with that of Drosophila dominant lethal test in terms of the concentrations at which equal clastogenic effect was seen. This comparison made it possible to conclude that the micronucleus test in mice was able to respond to much lower phthalate concentrations, as compared with the test in Drosophila. The results provided the evidence of capacity of dimethyl terephthalate to cause alterations of genetical structures in both somatic and germinal cells of two highly organized species in vivo.

Animals

[Specificity of mutagenic effect of N-nitroso-N-methylurea and relation between its mutagenic activity and carbamoylating properties].

Significance of carbamoylation for mutagenic effects of N-nitroso-N-methyl-urea (NMU) on the CHO-AT3-2 cell line of Chinese hamster was studied. True point mutations occurred, due to alkylation. Carbamoylation combined with alkylation, or carbamoylation after alkylation induced the increase in other types of gene mutations as well as micro- and macroaberrations. These effects may be explained by the synergistic effect of alkylation and carbamoylation. Possible mechanisms and levels of interaction between alkylation and carbamoylation are discussed.

Animals

[Modifying action of carbamoylation reaction on mutagenic and toxic effects of alkylating compounds and heavy metal salts].

Using mammalian somatic cells (CHO-AT3-2) we have demonstrated a synergistic effect of ethyl methane sulfonate and a carbamoylating agent, potassium cyanate. Potassium cyanate aggravated the toxic action of EMS and the induction of predominantly micro- and macroaberrational mutation, whereas the rate of point mutations of the base substitution type was not affected. No synergistic effect was observed when potassium cyanate was used in combination with heavy metal salts, regardless of the test employed.

Alkylating Agents

[Effect of alkylation and carbamoylation on the characteristics of genetic damage to mammalian somatic cells cultured in vitro].

Genetic effects of alkylation alone and combined with carbamoylation were studied following treatment of CHO-AT3-2 Chinese hamster cell line with N-nitroso-N-methylurea for 7 and 60 min. Gene mutations at HGPRT and Na+/K+-ATPase loci, micronuclei, cells with fragmented nuclei and lethality caused by NMU were recorded. Prolonged exposure to the mutagen made these effects more pronounced, particularly the fragmented nuclei and cell death. The combined action of the two mechanisms, therefore, enhanced the mutagenic effects of alkylation and expanded the range of DNA lesions towards greater incidence of gross damage to chromosomes and chromatids.

Animals

[Characteristics of mutagenesis induced by nitrosomethylurea in a mammalian multilocus system in vitro].

The mutagenic effect of short- and long-term MNU exposition causing alkylation and that combined with carbamoylation, correspondingly, at the four specific gene loci of the CHO-AT3-2 Chinese hamster line was studied. The increase both in MNU mutagenic effects and in the range of induced changes resulted from intensification of carbamoylating processes. True point mutations occurred mainly on alkylation. When carbamoylation is increased, the quantity and variety of mutations change towards accumulation of the number of other genetic lesions, for example, frameshift mutations and deletions.

Adenine Phosphoribosyltransferase

[Mutagenic action of cadmium chloride in mammals].

The mutagenic effect of cadmium chloride on somatic cells of F1 hybrid mice CBA X C57B1/6J in vivo and on an established line of CHO-ATZ-2 Chinese hamster cells in vitro has been studied. The induction of micronuclei has been demonstrated in mouse marrow cells as well as induction of point mutations at loci controlling the synthesis of hypoxanthine-phosphoribosyltransferase, thymidine kinase, adenine phosphoribosyltransferase and the resistance of Na+/K+ ATPase to ouabain in the cell line CHO-AT-2. A peak of mutagenic activity under the action of subtoxic doses of cadmium chloride has been revealed.

Animals

[Comparative study of the antimutagenic activity of diphenols].

Comparative study of the ability of three diphenols (pyrocathechol, resorcinol and hydroquinone) to inhibit the mutagenic activity of benzo(a)pyrene was carried out using the test for micronuclei account in mice polychromatic erythrocytes. It was suggested that the antimutagenic activity of diphenols used is mostly due to isomeric effect, i.e. the position of hydroxy-groups in molecules of diphenols.

Animals

[Relation of the antimutagenic activity of simple phenols to the number of hydroxyl groups].

The influence of mono-phenol, di-resorcinol and tri-pyrogallol hydroxyl groups of simple unsubstituted phenols on the mutagenic potentials of benzo(a)pyrene was studied in vivo (micronuclear test on bone marrow polychromatic erythrocytes) and in vitro (test of direct point mutations at V79/HGPRT system induced by metabolic activation by mouse liver microsomal enzymes). The phenols decreased the mutagenic activity of benzo(a)pyrene in in vivo tests, with pyrogallol being the most active, it followed by resorcinol and phenol. The mixtures of benzo(a) pyrene + pyrogallol and benzo(a)pyrene + resorcinol were significantly less mutagenic in in vitro tests than benzo(a)pyrene and benzo(a)pyrene + phenol.

Animals

[Effect of antioxidants on the carcinogenic and mutagenic activity of benzo[a]pyrene].

The changes in toxic, mutagenic and carcinogenic activities of benzo(a)pyrene (BP) in combination with two new phenolic antioxidants, phenosan-acid and -ester, were studied. Although both phenols investigated were characterized by marked toxic and mutagenic activity, their combination with BP appeared to protect mammalian cells against the action of the carcinogenic substance. A distinct correlation between inhibition of the mutagenic and toxic activities of BP and the dose of antioxidants was observed. The effect of phenosans on skin carcinogenesis induced by BP depended to a larger degree on the conditions of application of test substances. When combined applications of BP and antioxidants to the skin of mice were used, phenosans suppressed carcinogenesis, thus prolonging the latent period of tumor induction. When two-stage scheme of carcinogenesis was applied, a tendency for development predominantly benign skin tumors under the influence of antioxidants was noted. The use of the new phenolic antioxidants--phenosan-acid and -ester--seems to offer advantage in reducing mutagenicity and carcinogenicity of polycyclic aromatic hydrocarbons.

Animals

[Experimental study of the antimutagenic properties of 5-methylresorcinol].

A study was made of the effect of 5-methylresorcinol (5-MR) on mutagenic activity of benzo(a)pyrene (BP) and of the action of gamma-radiation in in-vitro and in-vivo systems. The induction of direct gene mutations in Chinese hamster cells V-79 and micronuclei in mouse bone marrow reticulocytes was efficiently suppressed by 5-MR treatment. The antimutagenic activity of 5-MR can be explained by inhibition of free-radical processes.

Animals

[Phenthiuram induction of micronuclei in mammalian somatic cells].

Genotoxic effects of the preparative-form phenthiuram on the induction of micronuclei in cultured Chinese hamster V-79 cells and polychromatic erythrocytes of mouse bone marrow have been studied. The phenthiuram induced cytogenetic effects in cultured somatic cells without metabolic activation being only in toxic concentrations. Similar effects were observed in polychromatic erythrocytes after treatment with subtoxic concentrations.

Animals

[Cypermethrin induction of micronuclei in mammalian somatic cells].

The genotoxic effects of the preparative cypermethrin form on the induction of micronuclei in cultured Chinese hamster V-79 cells and polychromatic erythrocytes of mouse bone marrow have been studied. The cypermethrin has induced micronuclei in cultured cells without metabolic activation in toxic concentrations, similar effects being observed in polychromatic erythrocytes after treatment with subtoxic concentrations.

Animals