19 research outputs found

    FIRST DATA ON AQUATIC MITES (ACARI) OF INLAND WATER BODIES OF WEST SPITSBERGEN, SVALBARD

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    This paper presents the first results of a study on the aquatic mites (Acari) from the inland water bodies of West Spitsbergen, Svalbard. Six mite species have been found: namely, the oribatids Camisia foveolata Hammer, 1955 and Ameronothrus lineatus (Thorell, 1871); the gamasid mite Halolaelaps sp.; as well as the halacarids Halacarellus sp., Isobactrus levis (Viets, 1927) and Rhombognathides spinipes (Viets, 1933). The latter two species are new to the fauna of Svalbard. No true freshwater mites (Hydrachnidia) have been identified. A preliminary comparison of the inland aquatic acarofauna of Svalbard with the fauna of other Arctic regions has been conducted. The entire halacarid mite fauna of Svalbard (13 species), including both inland water species and true marine ones from the surrounding seas, can be characterized as rather regionally specialized and mainly cryophilic. DOI: 10.21684/0132-8077-2017-25-2-181-18

    Expression of peroxiredoxin 1, 2, 3, and 6 genes in cancer cells during drug resistance formation

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    We studied the expression of peroxiredoxin genes (PRDX1, PRDX2, PRDX3, and PRDX6) in human erythroleukemia K652, human breast carcinoma MCF-7, and human ovarian carcinoma SKOV-3 cells during cisplatin resistance development. It was found that drug resistance formation was accompanied by a significant increase in the expression of PRDX1, PRDX2, PRDX3, PRDX6 genes in all cancer cell strains, which confirms the important contribution of redox-dependent mechanisms into the development of cisplatin resistance of cancer cells. © 2012 Springer Science+Business Media New York

    Expression of genes of glutathione transferase isoforms GSTP1-1, GSTA4-4, and GSTK1-1 in tumor cells during the formation of drug resistance to cisplatin

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    We studied the expression of genes encoding glutathione-S-transferase isoforms GSTP1-1, GSTA4-4, and GSTK1-1 during the development of the resistance of human erythroleukemia (K562), mammary adenocarcinoma (MCF-7) and ovary adenocarcinoma (SKOV-3) cells to cisplatin (CDDP). It was found that drug resistance development in all three strains of tumor cells is associated with signifi cant increase in hGSTP1 and hGSTA4 gene expression, whereas increased hGSTK1 gene expression was detected only in resistant K562/CDDP and MCF-7/CDDP cells. © 2012 Springer Science+Business Media New York

    Redox-Dependent Expression of Genes Encoding NADPH Oxidase 5 and the Key Antioxidant Enzymes during Formation of Drug Resistance of Tumor Cells to Cisplatin

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    Expression of genes that plays a significant role in the control of cellular redox homeostasis was studied during the development of drug resistance of human ovarian adenocarcinoma SKOV-3 cells to cisplatin. It was found that the development of drug resistance was accompanied by enhanced expression of the genes encoding the key antioxidant enzymes (SOD2, CAT, GPX1, and HO-1) and transcription factor Nrf2, as well as reduced expression of the gene encoding NOX5 isoform of NADPH oxidase. The results testify to redox-dependent development of the adaptive antioxidant response as an important process in the mechanism of formation of resistance to cisplatin. © 2018, Springer Science+Business Media, LLC, part of Springer Nature

    Expression of peroxiredoxin 1, 2, 3, and 6 genes in cancer cells during drug resistance formation

    No full text
    We studied the expression of peroxiredoxin genes (PRDX1, PRDX2, PRDX3, and PRDX6) in human erythroleukemia K652, human breast carcinoma MCF-7, and human ovarian carcinoma SKOV-3 cells during cisplatin resistance development. It was found that drug resistance formation was accompanied by a significant increase in the expression of PRDX1, PRDX2, PRDX3, PRDX6 genes in all cancer cell strains, which confirms the important contribution of redox-dependent mechanisms into the development of cisplatin resistance of cancer cells. © 2012 Springer Science+Business Media New York

    Trx/TrxR system in redox-dependent regulation under development of cisplatin resistance in cancer cells

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    Trx/TrxR-regulatory redox pathways may be the significant part of key events in the stress response and/or resetting redox homeostasis resulted in the change of most vital functions of cells, including proliferation, differentiation, apoptosis. Here we studied a level of Trx/TrxR activity and cellular redox-dependent changes during the development of resistance in human ovarian carcinoma SKOV-3 cells to cisplatin that possesses prooxidant effect. Increase of TRX1, TRXDR1, TRXDR2 gene expression as well as Trx and TrxR activity was found under formation of cancer cell resistance. The alteration of Trx/TrxR system was detected together with a change of the balance ROS/antioxidants in favor of growth of antioxidant state due to increase of key antioxidant enzymes gene expression (SOD2, CAT, GPX1, HO-1) and decrease of NADPH oxidase (NOX5) expression. Apoptosis suppression and much smaller extent of ASK1 and JNK1 phosphorylation were observed in resistant SKOV3/CDDP cells in contrast to the wild cells under H2O2 treatment. The results testify in favor of the important role of Trx/TrxR system in the rise of adaptive antioxidant response under formation of cisplatin resistance in cancer cells. The publication was prepared with the support of the «RUDN University Program 5-100»

    Expression of genes of glutathione transferase isoforms GSTP1-1, GSTA4-4, and GSTK1-1 in tumor cells during the formation of drug resistance to cisplatin

    No full text
    We studied the expression of genes encoding glutathione-S-transferase isoforms GSTP1-1, GSTA4-4, and GSTK1-1 during the development of the resistance of human erythroleukemia (K562), mammary adenocarcinoma (MCF-7) and ovary adenocarcinoma (SKOV-3) cells to cisplatin (CDDP). It was found that drug resistance development in all three strains of tumor cells is associated with signifi cant increase in hGSTP1 and hGSTA4 gene expression, whereas increased hGSTK1 gene expression was detected only in resistant K562/CDDP and MCF-7/CDDP cells. © 2012 Springer Science+Business Media New York
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