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Biomedical subjects

G D Zasukhina

Publications and source records attributed to G D Zasukhina.

At least 19 recordsLinked to original sources
PubMed2006

Antimutagenic characteristics of new diazacrown compounds with N-carboxyalkyl substitutes.

Two new benzodiaza-15-crown-5 compounds containing two N-hydroxycarbonylmethyl or N-hydroxycarbonylpropyl substitutes were synthesized. The first of these compounds exhibited more pronounced protective effects towards human cells according to criteria of primary DNA injury and cell survival after exposure to gamma-radiation and CdCl2; by antimutagenic activity this compound was comparable to garlic extract. The antimutagenic effect of these compounds was realized not through the antioxidant mechanism.

Antimutagenic Agents↗
PubMed2005

[Mechanisms of human cell protection associated with genetic polymorphism].

Systems ensuring protection of human cells against endogenous and exogenous mutagenic factors are considered in terms of genetic polymorphism. Some protection mechanisms are described, including those connected with capturing free radicals, biotransformation of xenobiotics, excision repair of DNA damage (excision of nitrous bases, nucleotides, mismatch repair). A special section is devoted to some issues of using antimutagens in context of genetic polymorphism. The problem of adaptive response is discussed, providing evidence for independence (in some cases) of DNA repair systems and the formation of adaptive response. Some results of the author obtained many years ago but still relevant are presented.

DNA Damage↗
PubMed2003

Antimutagenic and antioxidant activities of crown compounds in comparison with the effects of garlic extract.

Antimutagenic activity of N-carboxyalkyl derivatives of aza- and benzoazacrown compounds was revealed and antimutagenic activity of garlic extract was confirmed. Specific genoprotective effect of crown compounds towards the effects of various mutagens was demonstrated. The antimutagenic effect of these compounds was not realized via antioxidant mechanisms, while the protective effect of garlic extract was associated with its antioxidant and reparative activities.

Antimutagenic Agents↗
PubMed2003

[Differentiation of activity of a superoxide dismutase inhibitor in human cells exposed to radiation, chemical mutagens and radioadaptive response].

The superoxide dismutase (SOD) inhibitor, TRIEN, which enhanced the formation of gamma-induced DNA breaks in cells of healthy donors and patients with Marfan syndrome and Bloom syndrome (repair-defective hereditary diseases), had virtually no effect on the formation of radioadaptive response (RAR) in these systems. Similar results were obtained in studies on cell survival: TRIEN facilitated mortality in cells irradiated with gamma-rays but did not affect RAR formation. TRIEN also increased the deleterious effect of CdCl2, which indicates that SOD apparently plays a certain role in cell defence against this mutagen.

Bloom Syndrome↗
PubMed2002

[Modification of repair DNA synthesis in mutagen-treated human fibroblasts during adaptive response and the antimutagenic effect of garlic extract].

Repair DNA synthesis (RDS) in human fibroblasts during the adaptive responses (ARs) induced by cadmium chloride (CdCl2), gamma-radiation, and 4-nitroquinoline-1-oxide (4NQO) was compared in cells pretreated and not pretreated with garlic extract. The RDS was increased during the ARs induced CdCl2 and gamma-irradiation. Garlic extract stimulated RDS in cells treated by the same mutagens. 3-Aminobenzamide (3AB), an inhibitor of poly(ADP-ribose) polymerase, decreased the RDS rate in cells treated with CdCl2 and gamma-irradiation but had no significant effect on cells treated with 4NQO. It was demonstrated that DNA repair was involved into cell protection in different ways in the cases of antimutagen treatment and AR.

4-Nitroquinoline-1-oxide↗
PubMed2002

[Comparison of the protective effect of garlic extract and cell defense during adaptive response].

The resistance of human cell DNA to damaging doses of CdCl2 or gamma radiation has been investigated after pretreatment with garlic extract (GE) or with adaptive doses of the same mutagens. The adaptive response (AR) and pretreatment with GE stabilize the DNA structure in a similar way. In experiments with 4-nitroquinoline-1-oxide (4-NQO), GE does not stabilize DNA structure but increases the rate and volume of repair of induced breaks. 3-Aminobenzamide (3-AB) increases the number of DNA breaks induced in experiments with CdCl2, gamma radiation, and 4-NQO. This suggests that poly(ADP-ribose)polymerase participates defense of cells from mutagens. Thus, it has been demonstrated that cell defense from CdCl2 or gamma radiation in experiments with GE and AO is mediated by stabilization of DNA structure and in experiments with 4-NQO, by activation of repair of DNA breaks induced.

4-Nitroquinoline-1-oxide↗
PubMed2002

[The genotoxic effect of gunshot wounds].

Evidence for alterations in chromosomes of experimental animals (rats) and humans after gunshot wounds is presented. The rate of chromatid exchanges induced by gunshot wounds in humans depend on the saturation of body tissues with ascorbic acid. It is assumed that free-radical processes underlie the deleterious effect of gunshot wounds on chromosomes.

Animals↗
PubMed2001

Individual sensitivity to genotoxic effects of nickel and antimutagenic activity of ascorbic acid.

Cytotoxicity of nickel compounds was studied by stimulating the repair synthesis of DNA and counting lymphocyte micronuclei in workers of smelting shop of copper-nickel sulfide processing plant. Nickel content in the organism was evaluated by its concentrations in hair. Therapy with ascorbic acid (1 g/day for 1 month) led to a significant decrease in the number of micronuclei. The number of micronuclei before and after ascorbic acid treatment varied within a wide range in different individuals.

Air Pollutants, Occupational↗
PubMed2001

[Differences in individual sensitivity to the antimutagenic effect of retinol in lymphocytes from workers in contact with nickel compounds].

Individual sensitivity to nickel compounds was studied in workers employed in nickel industry. The mutagen sensitivity was inferred from the number of sister chromatid exchanges (SCEs), which was used to characterize the structural alterations of the chromosomes in workers' lymphocytes before and after administration of retinol for a month. The SCE number decreased after retinol administration in nine out of eleven workers.

Antimutagenic Agents↗
PubMed2000

[A defense mechanism of human cells in the radioadaptive response and antimutagenic activity of interferon has common paths].

The radioadaptive response was assessed by the chromosome aberration test in lymphocytes of humans with hereditary diseases of connective tissue, which were earlier characterized as repair-deficient: Marfan syndrome (SM), Elers-Danlos syndrome (E-D), and homocystinurea (HCU). The radioadaptive response was observed in cells of patients with Marfan syndrome and Elers-Danlos syndrome but not in cells of patients with homocystinurea. Parameters of cell protection against gamma-irradiation at radioadaptive response were similar to those obtained in cells pretreated with interferon. These data indicate, first, the possibility that repair pathways and the radioadaptive response are independent and second, that there are common pathways of protection upon radioadaptive response and the antimutagenic action of interferon.

Adaptation, Physiological↗
PubMed1998

[Repair processes in human cultured cells upon exposure to nickel salts and their modification].

The genetic activity of nickel sulfate was estimated from the viability, decreased DNA replication, and increased DNA repair synthesis in cultured human fibroblasts and peripheral blood lymphocytes. All but the viability tests showed the mutagenic effect of nickel sulfate. Pretreatment with ascorbic acid modified DNA repair synthesis and increased the viability of lymphocytes treated with nickel sulfate.

Cell Survival↗
PubMed1997

[Formation of sister chromatid exchanges and reparative DNA synthesis in workers exposed to nickel compounds].

In workers from a nickel processing plant, residents of the surrounding industrial zone, and a control group, levels of sister chromatid exchanges (SCE, 33 individuals) and DNA repair synthesis (DRS, 79 individuals) were estimated. Individual variations in SCE level did not correlate to the duration of exposure to nickel compounds or the level of pollution. A statistically significant increase of SCE level among smokers compared to nonsmokers was revealed. Workers exposed to nickel compounds were demonstrated to have a statistically significant increase in the inhibition of DNA repair synthesis.

Adult↗
PubMed1997

[Comparative study of DNA-repair ability of lymphocytes from systemic lupus erythematosus and rheumatoid arthritis patients].

Induction of DNA breaks with 4-NQO and their resynthesis in the cultivated lymphocytes of peripheral blood of 23 patients with systemic lupus erythematosus (SLE) and 12 patients with rheumatoid arthritis (RA) were studied by the method of hydroxyapatite column chromatography of cell lysates. The number of spontaneous DNA breaks was shown to increase in 48% of patients with SLE and in 42% of patients with RA, compared to that in the control. Inhibition of the repair process was observed in 35% of patients with SLE and in 17% of patients with RA. Complete repair of DNA breaks was observed in 67% of patients with RA and only in 26% of patients with SLE.

4-Nitroquinoline-1-oxide↗
PubMed1996

[Enhanced reactivation and induced mutagenesis of vaccinia virus in repair-defective cells of homocystinuria].

Two lines of fibroblasts isolated from patients with homocystinuria were characterized by the test of vaccinia virus host-cell reactivation. Xeroderma pigmentosum cells and normal fibroblasts were used as a control. Reduced host cell reactivation of the virus and an enhanced level of induced virus mutations in comparison with normal cells were revealed in homocystinuria cells after 4NQO and gamma-ray treatment. Enhanced reactivation and a corresponding reduced level of gamma-induced mutagenesis were found in preirradiated normal cells and in the xeroderma pigmentosum cells. The level of enhanced reactivation of the virus was virtually the same in preirradiated and nonirradiated homocystinuria cells, while the level of induced mutagenesis was reduced in both cells. This indicates the difference in the capability of the virus system for enhanced reactivation to repair potentially lethal and premutational DNA damages.

4-Nitroquinoline-1-oxide↗