[Modification of repair DNA synthesis in mutagen-treated human fibroblasts during adaptive response and the antimutagenic effect of garlic extract]. / Modifikatsiia reparativnogo sinteza DNK pri adaptivnom otvete i vozdeistvii antimutagena-chesnochnogo ékstrakta v fibroblastakh cheloveka, obrabotannykh mutagenami.

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.

[Enhanced reactivation and induced mutagenesis of vaccinia virus in repair-defective cells of homocystinuria]. / Izuchenie povyshennoi reaktivatsii i indutsirovannogo mutageneza virusa ospovaktsiny v reparatsionno-defektnykh kletkakh gomotsitinurii.

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.

[Dna repair activity in children exposed to small doses of ionizing radiation as a result of the accident at the Chernobyl nuclear power station]. / Reparativnaia aktivnost' DNK u detei, podverzhennykh vozdeistviiu malykh doz ioniziruiushchego izlycheniia v rezultate avarii na Chernobyl'skoi AES.

The repair activity of DNA was studied by variola vaccine virus reactivation and induced mutagenesis tests in the peripheral blood lymphocytes of children living in areas with an increased level of ionizing radiation due to breakdown at the Chernobyl' nuclear power station. A more profound repair disturbance was revealed in children living on strictly controlled territories and born after the disaster, compared to those born before it, and children living in areas where the radiation level does not exceed background values. The disturbances were characterized by increased induced mutagenesis and decreased reactivation of the variola vaccine virus. No changes in the degree of DNA repair synthesis were registered in any of the groups studied.

[The radioadaptive response in the lymphocytes of schizophrenia patients]. / Radioadaptivnyi otvet v limfotsitakh bol'nykh shizofreniei.

Radioadaptive response in cells from three patients was studied by induction of structural chromosome aberrations. Radioadaptive response was revealed in lymphocytes of all three patients. Coefficient of protection was 59.0% and did not differ from this after cell pretreatment with interferon. It is suggested the similarity or identity of mechanism of radioadaptive response and of interferon antimutagenic action which was implemented by non-repair way.

[Absence of adaptive DNA repair in xeroderma pigmentosum cells]. / Otsutstvie adaptivnoi reparatsii DNK v kletkakh pigmentnoi kserodermy.

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.

[Interferon as a stimulator of DNA repair in patients with xeroderma pigmentosum]. / Interferon kak stimuliator reparatsii DNK u bol'nykh xeroderma pigmentosum.

Natural leucocyte interferon (IF) upon injection to two patients affected with Xeroderma pigmentosum for three weeks stimulated the inhibited DNA replication and Host reactivation at the level of healthy donors. Tigasol--the drug used traditionally for the treatment of diseases caused by Xeroderma pigmentosum proved less effective than IF.

[Protective effect of ascorbic acid in cells of people exposed to cobalt chloride]. / Zashchitnoe deistvie askorbinovoi kisloty v kletkakh liudei, kontaktiruiushchikh s khloridom kobal'ta.

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.

[The preservation of a DNA repair disorder in continuous-line fibroblasts obtained from gout patients]. / Sokhranenie narushemiia reparatsii DNK v perevivaemykh fibroblastakh, poluchennykh ot bol'nykh podagroi.

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.

[Decrease in repair processes in lymphocytes of workers exposed to heavy metals]. / Snizhenie reparativnykh protsessov v limfotsitakh rabochikh, kontaktiruiushchikh s tiazhelymi metallami.

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.

[Mechanisms of disruption of DNA in human cells. Mutagenesis of a virus in xeroderma pigmentosum cells as an indicator of a defect in DNA repair]. / Mekhanizmy narushenii reparatsii DNK v kletkakh cheloveka. Mutagenez virusa v kletkakh pigmentnoi kcerodermy kak pokazatel' defekta reparatsii DNK.

Lymphocytes of two patients with Xeroderma pigmentosum, their mothers and cell lines isolated from the third patient were examined. The reaction of vaccinia virus treated with mutagens, the index of virus-induced mutagenesis and DNA repair synthesis were the criteria of estimation of cell repair activity. Significant inhibition of DNA repair synthesis was detected in cells of all the patients observed (primary and established lines) in the experiments with UV-irradiation and 4-nitroquinoline-4-oxide. These indexes correlated with decreased virus reactivation and increased level of virus-induced mutagenesis. Inhibition of DNA repair synthesis was also revealed in lymphocytes of both mothers. These data claim a possibility of discovering heterozygotes, the carriers of mutant genes. The data on virus-induced mutagenesis serve as a simple test for detection of DNA repair disorders.

[Analysis of familial cases of gout using tests for DNA repair]. / Analiz semeinykh sluchaev podagry pri ispolzovanii testov na reparatsiiu povrezhdenii DNK.

As many as 8 families suffering from gout were examined with the use of four tests for the repair of DNA damages. The criteria applied for the assessment of the reparative activity made it possible to identify in total or in different combinations the inhibition of the repair in the lymphocytes of all the probands examined. The use of 1-3 procedures revealed the repair defects in all the families, namely in the lymphocytes of the probands' relatives. Based on this fact an attempt has been made to identify possible carriership of the "pathological" genes in the proband's relatives, which in future will make it possible to develop approaches to the identification of the genetic markers of the disease as well as to the disease prevention.

[Mechanisms of DNA repair disorders in human cells. Genome instability in lymphocytes of patients with myopathy related to DNA repair disorders]. / Mekhanizmy narushenii reparatsii DNK v kletkakh cheloveka. Nestabil'nost' genoma v limfotsitakh bol'nykh miopatiiami, sviazannaia s narusheniem reparatsii DNK.

Increased level of cytogenetic damages was observed in lymphocytes of 10 patients with muscular dystrophy (Duchenne, Erba, Landuzi--Degerin). Analysis of DNA repair synthesis revealed inhibition of this process in lymphocytes of 10 patients observed. On the other hand, decreased reactivation of vaccinia virus and increased level of virus mutagenesis induced by 4-nitroquinoline-1-oxide and bleomycin was noted in the experiments with lymphocytes of 3 patients observed.

[Chromosomal instability related to disordered replication and repair processes of DNA synthesis in the cells of patients with gouty nephropathy]. / Khromosomnaia nestabil'nost', sviazannaia s narusheniem protsessov replikatsii i reparatsii sinteza DNK, v kletkakh bol'nykh podagricheskoi nefropatiei.

Lymphocytes of patients with gouty nephropathy were investigated using the criteria of sister chromatid exchanges (SCE) formation, rapidity of generation, virus reactivation, detection of the level of virus mutagenesis and DNA repair and replication synthesis in the experiments with some mutagens. Disorders, according to these criteria, were observed in the cells of all the patients. Cells of patients with gouty nephropathy may be used as a model to study DNA repair and replication mechanisms.

[Disordered DNA repair in the lymphocytes of patients with schizophrenia depending on the form of the course of the disease]. / Narushenie reparatsii DNK v limfotsitakh bol'nykh shizofreniei v zavisimosti ot formy techeniia zabolevaniia.

Employing the appropriate technique the authors have examined lymphocytes of 26 patients suffering from schizophrenia of different types. The study has shown distinct disorders of DNA reparation associated with this disease, which is suggestive of deficiency or noncoordination of the enzymatic system explained by mutations in corresponding genes. Disorders of DNA reparation have until recently been known to be associated only with hereditary diseases.

[Disorders of repair processes in the lymphocytes of schizophrenia patients, cultured in vitro]. / Narusheniia protsessov reparatsii v limfotsitakh bol'nykh shizofreniei, kul'tiviruemykh in vitro.

Repair disorders of DNA damage induced by gamma-radiation and 4-nitroquinoline-1-oxide treatment in cultivated lymphocytes of patients with schizophrenia. 13 criteria were used for estimation of repair activity (reactivation of viral host cells) repair synthesis, reparation of DNA breaks, formation of spontaneous and induced sister chromatid exchanges.