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Statements

Subject Item
n2:RIV%2F61989592%3A15110%2F10%3A10212701%21RIV11-GA0-15110___
rdf:type
skos:Concept n15:Vysledek
dcterms:description
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. 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.
dcterms:title
Dehydrosilybin attenuates the production of ROS in rat cardiomyocyte mitochondria with an uncoupler-like mechanism Dehydrosilybin attenuates the production of ROS in rat cardiomyocyte mitochondria with an uncoupler-like mechanism
skos:prefLabel
Dehydrosilybin attenuates the production of ROS in rat cardiomyocyte mitochondria with an uncoupler-like mechanism Dehydrosilybin attenuates the production of ROS in rat cardiomyocyte mitochondria with an uncoupler-like mechanism
skos:notation
RIV/61989592:15110/10:10212701!RIV11-GA0-15110___
n3:aktivita
n18:P n18:Z
n3:aktivity
P(GA303/08/0658), Z(AV0Z50110509), Z(AV0Z50200510), Z(MSM6198959216)
n3:cisloPeriodika
6
n3:dodaniDat
n10:2011
n3:domaciTvurceVysledku
n17:1030957 n17:3443825 n17:4594266
n3:druhVysledku
n12:J
n3:duvernostUdaju
n19:S
n3:entitaPredkladatele
n5:predkladatel
n3:idSjednocenehoVysledku
253157
n3:idVysledku
RIV/61989592:15110/10:10212701
n3:jazykVysledku
n6:eng
n3:klicovaSlova
Dehydrosilybin; Respiration uncoupling; Protonophore; Mitochondria; Cardiomyocytes; Reactive oxygen species
n3:klicoveSlovo
n4:Cardiomyocytes n4:Reactive%20oxygen%20species n4:Dehydrosilybin n4:Mitochondria n4:Protonophore n4:Respiration%20uncoupling
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[72348C66B072]
n3:nazevZdroje
Journal of Bioenergetics and Biomembranes
n3:obor
n7:CE
n3:pocetDomacichTvurcuVysledku
3
n3:pocetTvurcuVysledku
7
n3:projekt
n9:GA303%2F08%2F0658
n3:rokUplatneniVysledku
n10:2010
n3:svazekPeriodika
42
n3:tvurceVysledku
Ježek, Jan Gažák, Radek Modrianský, Martin Jabůrek, Martin GABRIELOVÁ, Eva Vostálová, Jitka Křen, Vladimír
n3:zamer
n16:AV0Z50110509 n16:AV0Z50200510 n16:MSM6198959216
s:issn
0145-479X
s:numberOfPages
10
n11:organizacniJednotka
15110