Dehydrosilybin attenuates the production of ROS in rat cardiomyocyte mitochondria with an uncoupler-like mechanism

0355107 - FGÚ 2011 RIV US eng J - Journal Article
Gabrielová, E. - Jabůrek, Martin - Gažák, Radek - Vostálová, J. - Ježek, Jan - Křen, Vladimír - Modrianský, M.
Dehydrosilybin attenuates the production of ROS in rat cardiomyocyte mitochondria with an uncoupler-like mechanism.
Journal of Bioenergetics and Biomembranes. Roč. 42, č. 6 (2010), s. 499-509. ISSN 0145-479X. E-ISSN 1573-6881
R&D Projects: GA ČR(CZ) GA303/08/0658
Institutional research plan: CEZ:AV0Z50110509; CEZ:AV0Z50200510
Keywords : Reactive oxygen species * Cardiomyocytes * Dehydrosilybin
Subject RIV: CE - Biochemistry
Impact factor: 3.637, year: 2010

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
Permanent Link: http://hdl.handle.net/11104/0193950