[New mechanisms of antimutagenic effect of interferon]. / Novye mekhanizmy antimutagennogo deistviia interferona.

A study was made of the antimutagenic effect of natural lymphoblastoid interferon and alpha 2-recombinant interferon against initial damages to DNA induced by 8-methoxypsoralen, activated by UV-light, in human peripheral blood. The crosslinking and uncrosslinking 8-methoxypsoralen monoadducts were shown to make different contribution to the biological effects in cells, that is, chromosome aberrations and sister chromatid exchanges. Both of the investigated interferons exhibited their protective effect with respect to crosslinking monoadducts only. The antimutagenic action of interferon was implemented by a non-repair way. It is suggested that the scavenging of active radicals is a possible mechanism of the protective action of interferon.

[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]. / Mekhanizmy narushenii reparatsii DNK v kletkakh chelovka. Soobshchenie IV. Interferon zashchishchaet DNK neinfitsirovannykh i khronicheski infitsirovannykh kletok cheloveka ot povrezhdenii, vyzyvaemykh khloristym kadmiem.

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.

[Mechanism of the antimutagenic action of dibunol]. / K voprosu o mekhanizme antimutagennogo deistviia dibunola.

In experiments with cultured V-79 Chinese hamster cells a study was made of the influence of dibunol on the level of gamma-radiation-induced micronuclei and sedimentation properties of cell nucleoids during ultracentrifugation in a neutral sucrose gradient. Protection of DNA molecule against the effects of both primary and secondary damages was found to be involved in the mechanism of the protective action of dibunol.

[Repair of DNA damage induced by gamma radiation and UV and gamma mimetics in virus-infected human cells]. / Reparatsiia povrezhdenii DNK, indutsirovannykh gamma-izlucheniem, UF- i gamma-mimetikami v infitsirovannykh virusami kletkakh cheloveka.

The method of chromatography of cell lysates on the columns with hydroxyapatite (HAP) and the method of ultracentrifugation of cell lysates in neutral sucrose gradient were used to study the mutagen-induced repair activity of human cells HEp-2 noninfected and chronically infected with measles and rubella viruses in order to determine the sedimentation properties of complexes containing DNA. Gamma-radiation, bleomycin, 4-nitroquinoline-1-oxide, and mitomycin C were used as DNA damaging agents. It was shown that the chronic infectious process inhibited repair of DNA damages induced by 4-nitroquinoline-1-oxide and mitomycin C and did not influence repair of DNA lesions caused by gamma-radiation and bleomycin.

[Difference in the capacity to repair DNA damage in human cells chronically infected with the rubella virus]. / Razlichie v sposobnosti k reparatsii povrezhdenii DNK kletok cheloveka, khronicheski infitsirovannykh virusom krasnukhi.

Centrifugation of cell lysates in alkaline sucrose gradients and chromatography on hydroxyapatite columns were used to demonstrate inhibition of reparation of mitomycin C-induced DNA damages at the stage of reunification of single-strand breaks of DNA in human HEp-2 cell cultures chronically infected with rubella virus. At the same time, reparation of single-strand breaks of DNA caused by bleomycin occurs with similar intensity both in chronically infected and noninfected HEp-2 cultures. The experimental results suggest that the chronic course of infection in human cells leads to disorders in reparative synthesis of cellular DNA and/or is due to disconnected effect of reparation enzymes in this system.

[Inhibition of the process of 4-nitroquinoline-1-oxide-induced DNA break repair in chronically virus-infected human cells]. / Ingibirovanie protsessa vossoedineniia razryvov DNK, indutsirovannykh 4-nitrokhinolin-1-oksidom v kletkakh cheloveka, khronicheski indutsirovannykh virusami.

Inhibition of DNA resynthesis after treatment of cell culture with 4-nitroquinoline-1-oxide was found to be due not to the induction of virus mutants repressing this system but to the selection in the cell population of cells predominantly with partially or completely defective system of reparation, or to the development of cellular reparative system because of the presence of viruses in the cell. In chronic infection of HEp-2 cells with tick-borne encephalitis, rubella, and rabies viruses the same phenomenon was observed, namely, inhibition of different stages of the reparation process, i.e. the mechanism of reparation is universal.