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Dehydrosilybin attenuates the production of ROS in rat cardiomyocyte mitochondria with an uncoupler-like mechanism
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SYSNO ASEP 0355107 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Dehydrosilybin attenuates the production of ROS in rat cardiomyocyte mitochondria with an uncoupler-like mechanism Author(s) Gabrielová, E. (CZ)
Jabůrek, Martin (FGU-C) ORCID, RID
Gažák, Radek (MBU-M) RID, ORCID
Vostálová, J. (CZ)
Ježek, Jan (FGU-C) RID, ORCID
Křen, Vladimír (MBU-M) RID, ORCID
Modrianský, M. (CZ)Source Title Journal of Bioenergetics and Biomembranes - ISSN 0145-479X
Roč. 42, č. 6 (2010), s. 499-509Number of pages 11 s. Language eng - English Country US - United States Keywords Reactive oxygen species ; Cardiomyocytes ; Dehydrosilybin Subject RIV CE - Biochemistry R&D Projects GA303/08/0658 GA ČR - Czech Science Foundation (CSF) CEZ AV0Z50110509 - FGU-C (2005-2011) AV0Z50200510 - MBU-M (2005-2011) UT WOS 000285753300010 DOI 10.1007/s10863-010-9319-2 Annotation Reactive oxygen species (ROS) originating from mitochondria are perceived as a factor contributing to cell aging. Silybin and dehydrosilybin, two polyphenolic compounds, display a plethora of biological effects generally ascribed to their known antioxidant capacity. When investigating the cytoprotective effects of these two compounds in the primary cell cultures of neonatal rat cardiomyocytes, we noted the ability of dehydrosilybin to de-energize the cells by monitoring JC-1 fluorescence. Experiments evaluating oxygen consumption and membrane potential revealed that dehydrosilybin uncouples the respiration of isolated rat heart mitochondria albeit with a much lower potency than synthetic uncouplers. We infer that the apparent uncoupler-like activity of dehydrosilybin is the basis of its ROS modulation effect in neonatal rat cardiomyocytes and leads us to propose a hypothesis on natural ischemia preconditioning by dietary polyphenols Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2011
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