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166 results on '"Zinovkin, R."'

10. Mitochondrial Targeting of Antioxidants

Author

Zinovkin, R. A., Bakeeva, L. E., Chernyak, B. V., Egorov, M. V., Isaev, N. K., Kolosova, N. G., Korshunova, G. A., Manskikh, V. N., Moshkin, M. P., Plotnikov, E. Y., Rogovin, K. A., Savchenko, A. Y., Zamyatnin, A. A., Jr., Zorov, D. B., Skulachev, M. V., Skulachev, V. P., and Laher, Ismail, editor

Published
2014
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25. Mitochondria-targeted plastoquinone derivatives as tools to interrupt execution of the aging program. 4. Age-related eye disease. SkQ1 returns vision to blind animals

Author

Neroev, V. V., Archipova, M. M., Bakeeva, L. E., Fursova, A. Zh., Grigorian, E. N., Grishanova, A. Yu., Iomdina, E. N., Ivashchenko, Zh. N., Katargina, L. A., Khoroshilova-Maslova, I. P., Kilina, O. V., Kolosova, N. G., Kopenkin, E. P., Korshunov, S. S., Kovaleva, N. A., Novikova, Yu. P., Philippov, P. P., Pilipenko, D. I., Robustova, O. V., Saprunova, V. B., Senin, I. I., Skulachev, M. V., Sotnikova, L. F., Stefanova, N. A., Tikhomirova, N. K., Tsapenko, I. V., Shchipanova, A. I., Zinovkin, R. A., and Skulachev, V. P.

Published
2008
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37. Age-associated murine cardiac lesions are attenuated by the mitochondria-targeted antioxidant SkQ1

Author

Manskikh, V. N., Gancharova, S., Nikiforova, I., Krasilshchikova, M. S., Shabalina, Irina G., Egorov, M. V., Karger, E. M., Milanovsky, G. E., Galkin, I. I., Skulachev, V. P., Zinovkin, R. A., Manskikh, V. N., Gancharova, S., Nikiforova, I., Krasilshchikova, M. S., Shabalina, Irina G., Egorov, M. V., Karger, E. M., Milanovsky, G. E., Galkin, I. I., Skulachev, V. P., and Zinovkin, R. A.

Abstract

Age-related changes in mammalian hearts often result in cardiac hypertrophy and fibrosis that are preceded by inflammatory infiltration. In this paper, we show that lifelong treatment of BALB/c and C57BL/6 mice with the mitochondria-targeted antioxidant SkQ1 retards senescence-associated myocardial disease (cardiomyopathy), cardiac hypertrophy, and diffuse myocardial fibrosis. To investigate the molecular basis of the action of SkQ1, we have applied DNA microarray analysis. The global gene expression profile in heart tissues was not significantly affected by administration of SkQ1. However, we found some small but statistically significant modifications of the pathways related to cell-to-cell contact, adhesion, and leukocyte infiltration. Probably, SkQ1-induced decrease in leukocyte and mesenchymal cell adhesion and/or infiltration lead to a reduction in age-related inflammation and subsequent fibrosis. The data indicate a causative role of mitochondrial reactive oxygen species in cardiovascular aging and imply that SkQ1 has potential as a drug against age-related cardiac dysfunction., AuthorCount:11

Published
2015
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47. A-to-I RNA Editing: A Contribution to Diversity of the Transcriptome and an Organism's Development.

Author

Zamyatnin, A., Lyamzaev, K., and Zinovkin, R.

Subjects
RNA editing, PATHOGENIC microorganisms, EUKARYOTIC cells, MESSENGER RNA, ADENOSINE deaminase, PROTOZOA, GENETIC polymorphisms, GENE expression, CELL membrane formation, CARRIER proteins, ONTOGENY
Abstract

The complexity of multicellular organisms requires both an increase in genetic information and fine tuning in regulation of gene expression. One of the mechanisms responsible for these functions is RNA editing. RNA editing is a complex process affecting the mechanism of changes in transcriptome sequences. The best studied example of this process is A-to-I RNA editing. On the organism's level, RNA editing plays a key role during ontogenesis and in the defense against pathogens. Disorders in A-to-I RNA editing lead to serious abnormalities. The importance of RNA editing increases with an increase in the organism's complexity. Correct RNA editing is an indispensable factor of an organism's development and probably determines the lifespan of higher eukaryotes. [ABSTRACT FROM AUTHOR]

Published
2010
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48. Effect of Ca2+ on programmed death of guard and epidermal cells of pea leaves.

Author

Kiselevsky, D. B., Kuznetsova, Yu. E., Vasil'ev, L. A., Lobysheva, N. V., Zinovkin, R. A., Nesov, A. V., Shestak, A. A., and Samuilov, V. D.

Subjects
PEAS, OSMOSIS, EPIDERMIS, EPITHELIUM, CELL nuclei
Abstract

The effect of Ca2+ on programmed death of guard cells (GC) and epidermal cells (EC) determined from destruction of the cell nucleus was investigated in epidermis of pea leaves. Ca2+ at concentrations of 1–100 μM increased and at a concentration of 1 mM prevented the CN—induced destruction of the nucleus in GC, disrupting the permeability barrier of GC plasma membrane for propidium iodide (PI). Ca2+ at concentrations of 0.1–1 mM enhanced drastically the number of EC nuclei stained by PI in epidermis treated with chitosan, an inducer of programmed cell death. The internucleosomal DNA fragmentation caused by CN− was suppressed by 2 mM Ca2+ on 6 h incubation, but fragmentation was stimulated on more prolonged treatment (16 h). Presumably, the disruption of the permeability barrier of plasma membrane for PI is not a sign of necrosis in plant cells. Quinacrine and diphenylene iodonium at 50 μM concentration prevented GC death induced by CN− or CN− + 0.1 mM Ca2+ but had no influence on respiration and photosynthetic O2 evolution in pea leaf slices. The generation of reactive oxygen species determined from 2′,7′-dichlorofluorescein fluorescence was promoted by Ca2+ in epidermal peels from pea leaves. [ABSTRACT FROM AUTHOR]

Published
2010
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49. Chitosan-induced programmed cell death in plants.

Author

Vasil'ev, L. A., Dzyubinskaya, E. V., Zinovkin, R. A., Kiselevsky, D. B., Lobysheva, N. V., and Samuilov, V. D.

Subjects
CELL death, CHITOSAN, CHROMATIN, PROPYL gallate, PROTEIN synthesis, CHEMICAL inhibitors
Abstract

Chitosan, CN−, or H2O2 caused the death of epidermal cells (EC) in the epidermis of pea leaves that was detected by monitoring the destruction of cell nuclei; chitosan induced chromatin condensation and marginalization followed by the destruction of EC nuclei and subsequent internucleosomal DNA fragmentation. Chitosan did not affect stoma guard cells (GC). Anaerobic conditions prevented the chitosan-induced destruction of EC nuclei. The antioxidants nitroblue tetrazolium or mannitol suppressed the effects of chitosan, H2O2, or chitosan + H2O2 on EC. H2O2 formation in EC and GC mitochondria that was determined from 2′,7′-dichlorofluorescein fluorescence was inhibited by CN− and the protonophoric uncoupler carbonyl cyanide m-chlorophenylhydrazone but was stimulated by these agents in GC chloroplasts. The alternative oxidase inhibitors propyl gallate and salicylhydroxamate prevented chitosan- but not CN−-induced destruction of EC nuclei; the plasma membrane NADPH oxidase inhibitors diphenylene iodonium and quinacrine abolished chitosan- but not CN−-induced destruction of EC nuclei. The mitochondrial protein synthesis inhibitor lincomycin removed the destructive effect of chitosan or H2O2 on EC nuclei. The effect of cycloheximide, an inhibitor of protein synthesis in the cytoplasm, was insignificant; however, it was enhanced if cycloheximide was added in combination with lincomycin. The autophagy inhibitor 3-methyladenine removed the chitosan effect but exerted no influence on the effect of H2O2 as an inducer of EC death. The internucleosome DNA fragmentation in conjunction with the data on the 3-methyladenine effect provides evidence that chitosan induces programmed cell death that follows a combined scenario including apoptosis and autophagy. Based on the results of an inhibitor assay, chitosan-induced EC death involves reactive oxygen species generated by the NADPH oxidase of the plasma membrane. [ABSTRACT FROM AUTHOR]

Published
2009
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