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Biomedical subjects

I M Vasil'eva

Publications and source records attributed to I M Vasil'eva.

At least 19 recordsLinked to original sources

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↗

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↗

[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↗

[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↗

[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↗

[Radio-adaptive response in repair-defective cells from patients with homocystinuria].

Two lines of fibroblasts isolated by skin biopsy from patients with homocystinuria were characterized as repair-defective cells. Preirradiation of these cells at low doses (0.1 Gy) and irradiation at high doses demonstrated their decreased ability to form radioadaptive response, in comparison with normal cells. Radioadaptive response did not differ from that of normal cells after chemical treatment with 4NQO and NG used as damaging agents. The method for detection of DNA breaks by means of hydroxyapatite column chromatography of cell lysates and the method of determining sister chromatid exchanges (SCE) were used.

Adaptation, Physiological↗

[Absence of adaptive DNA repair in xeroderma pigmentosum cells].

Adaptive repair is the restoration of chemically induced DNA breaks in human fibroblasts previously gamma-irradiated at low doses. The adaptive repair in xeroderma pigmentosum (XP) cells was compared to that in normal human fibroblasts. The obtained results suggest that the repair is inducible and error-free. Adaptive repair was not found in XP cells in experiments with 4-NQO. This is correlated with the presence of an excision repair defect in XP.

Cells, Cultured↗

[The preservation of a DNA repair disorder in continuous-line fibroblasts obtained from gout patients].

DNA repair was explored in continuous cells withdrawn from gout patients. The data obtained were compared to those on primary cells (lymphocytes) from the same patients. Two continuous lines of fibroblasts obtained from the biopsy material of patients suffering from gout were examined for stability of reparation defects on long cell passage. The studies were made with 4 to 12 passages of patients' fibroblasts. The use of criteria reflecting certain stages of DNA repair (reparative synthesis of DNA, formation of induced DNA ruptures and their resynthesis during cell postincubation, reactivation and induced mutagenesis of measles vaccine virus in patients' cells) allowed confirmation of repair defect stability in gout patients' cells on their long passage. Based on the data on preservation of the repair defect on cell passage it is concluded that gout patients demonstrate the genetically determined impairment of the synthesis of DNA repair enzymes participating in the recovery of DNA impairments induced by UV radiation or UV mimetics.

4-Nitroquinoline-1-oxide↗

[Protective effect of ascorbic acid in cells of people exposed to cobalt chloride].

The workers contacting with cobalt chloride for 10 years and more have been receiving 50 mg ascorbic acid for 30 days. DNA repair was analysed after this procedure in lymphocytes cultivated in vitro according to following criteria: reactivation and induced mutagenesis of vaccinia virus as well as formation of DNA breaks and their resynthesis upon treatment with cobalt chloride and 4-nitro-quinoline-1-oxide.

4-Nitroquinoline-1-oxide↗

[Mechanisms of disrupting DNA repair in human cells. IV. Interferon protects DNA of noninfected and chronically infected human cells from damage caused by cadmium chloride].

The protective activity of interferon on the cadmium chloride-treated human cells (Hep-2), infected chronically with meals virus and uninfected, was studied. It was found that cadmium chloride induced the formation of partially non-repairable DNA lesions. Decrease in cell repair activity was observed in the cells chronically infected with virus. Pretreatment of cells with interferon protected cell DNA from formation of DNA breaks and caused more effective resynthesis of DNA breaks.

Cadmium↗

[Decrease in repair processes in lymphocytes of workers exposed to heavy metals].

Mechanisms of DNA repair in lymphocytes of persons having occupational contact with heavy metal salts for at least 10 years were investigated. The long-term exposure to heavy metal salts did not result in development of mechanisms of adaptation to the respective metals, as shown by increased DNA sensitivity to these compounds and by decrease in the repair activity. However, in some cases, resistance to other mutagens, 4-NQO, in particular, was observed.

Cobalt↗