Антивирусный препарат изатизон не обладает мутагенным действием и стимулирует пролиферацию клеток иммунной системы На экспериментальных моделях изучено мутагенное действие антивирусного препарата изати зона, Показано, что он не обладает мутагенным эффектом как на уровне хромосомных аберра ций, так и в отношении частоты генных мутаций устойчивости кб-меркаптопурину. В культу ре клеток, инфицированных вирусом герпеса простого (тип I), наблюдали достоверное увеличе ние частоты хромосомных аберраций. Изатизон одновременно с ингибированием репродукции вируса снижал количество хромосомных аномалий до уровня контроля. Обнаружена стимуляция изатизоном пролиферативной активности лимфоцитов как в культуре клеток СЕМ-4, так и в опытах на цыплятах-Бройлерах 6, что коррелировало с увеличением продуктивности птиц. Предполагается, что антивирусное действие изатизона обусловлено его влиянием на инфициро ванные клетки, а также на клетки иммунной системы

To explain the tissue-selective expression patterns of a distinct subclass of glutathione S-transferase (GST), transgenic mice expressing EGFP under control of a 2 kb promoter sequence in the 5'-flanking region of the mGstm5 gene were produced. The intent of the study was to establish whether the promoter itself or whether posttranscriptional mechanisms, particularly at the levels of mRNA translation and stability or protein targeting, based on unique properties of mGSTM5, determine the restricted expression pattern. Indeed, the transgene expression was limited to testis as the reporter was not detected in somatic tissues such as brain, kidney or liver, indicating that the mGstm5 proximal promoter is sufficient to target testis-specific expression of the gene. EGFP expression was also more restricted vis-a-vis the natural mGstm5 gene and exclusively found in germ but not in somatic cells. Real-time quantitative PCR (qPCR) data were consistent with alternate transcription start sites in which the promoter region of the natural mGstm5 gene in somatic cells is part of exon 1 of the germ cell transcript. Thus, the primary transcription start site for mGstm5 is upstream of a TATA box in testis and downstream of this motif in somatic cells. The 5' flanking sequence of the mGstm5 gene imparts germ cell-specific transcription.

The mechanism of N-methyl-izatin-thiocarbazone (methisazone, Mel ВТ) antiviral activity has been studied on Ad 1-infected HEp2 and HeLa cells. Mel ВТ did not induce interferon and did not directly inhibit viral and cell translation. The adenoviral infection was not affected by recombinant human interferon a 2 (rIFN). Mel ВТ showed antiviral effect in AdI-infected HEp2 or HeLa cells when rIFN had added to HeLa cells or in the period of interferon induction during virus infection (in HEp2 cells). In the presence of this compound, the El A transcription was unchanged in infected cells as compared to untreated control, while early transcription was decreased, the beginning of viral replicationbeing retarded. Futhermore, the VAI RNA synthesis was also greatly suppressed.These effects were independent on interferon treatment and disappeared when MeIВТ had been added during the late phase of virus growth cycle. Actually, MeIВТ can induce the delay of VAI RNA transcription promoting interferon antiviral effect

In our earlier investigations it was discovered the mutagenic activity of two recombinant plasmids (pBR322ins and pAins) containing the human preproinsulin gene in cultivated somatic mammalian cells. The preproinsulin gene (allel-I) was able to function under its own promoter in different cell types since it lacked a regulatory element providing tissuespecific expression. Introduction of aframeshift mutation into the region of initiation of the translation of the transgene (allel-2) diminished the mutagenic effect of a corresponding recombinant plasmid on gene level In this work the mutagenic activity of the recombinant plasmids carrying allel-1 (pBR322ins) and allel-2 (pBR322insN) of the preproinsulin gene was studied using cytogenetic test. It was shown that the presence of allel-2 (that probably had altered expression of the transgene) in the recombinant plasmid structure decreased the level of induced chromosome breaks per cell. It was made a conclusion that not only viruses and their genes but also recombinant DNAs of nonviral origin are able to induce chromosome and gene mutations in mammalian cells. The mutagenic activity of studied recombinant plasmids depends on the level of expression of the transgenes in the cells.

The role of indole-3-acetic acid accumulation by alpha methyl trvptophaii-resistant mutants of Pseuciomonas savastanoi in gall formation on oleanders//Physiol. Plant Pathol-1978,-13, N 2.-P. 203-214. 10. Argobacterium Ti plasmid indoleacetic acid gene is required for crown gall oncogenesis/S.