Hort 2014 Biochimie: Difference between revisions
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|abstract=Elevated levels of oxidized low density lipoprotein (oxLDL) are considered to be one of the major risk factors for atherosclerosis and cardiovascular morbidity. The early stages of atherosclerosis are initiated by the accumulation of oxLDL and the induction of toxic effects on endothelial cells, resulting in endothelial dysfunction. The aim of this study was to investigate how diphenyl diselenide (DD), an organoselenium compound, protect vascular endothelial cells against the toxic effects of oxLDL in vitro. Our data showed that the treatment of bovine endothelial aortic cells (BAEC) with DD (0.1-1 ฮผM) for 24 h protected from oxLDL-induced reactive species (RS) production and reduced glutathione (GSH) depletion. Moreover, DD (1 ฮผM) per se improved the maximal mitochondrial respiratory capacity and prevented oxLDL-induced mitochondrial damage. In addition, DD could prevent apoptosis induced by oxLDL in BAEC. Results from this study may provide insight into a possible molecular mechanism underlying DD suppression of oxLDL-mediated vascular endothelial dysfunction. | |abstract=Elevated levels of oxidized low density lipoprotein (oxLDL) are considered to be one of the major risk factors for atherosclerosis and cardiovascular morbidity. The early stages of atherosclerosis are initiated by the accumulation of oxLDL and the induction of toxic effects on endothelial cells, resulting in endothelial dysfunction. The aim of this study was to investigate how diphenyl diselenide (DD), an organoselenium compound, protect vascular endothelial cells against the toxic effects of oxLDL in vitro. Our data showed that the treatment of bovine endothelial aortic cells (BAEC) with DD (0.1-1 ฮผM) for 24 h protected from oxLDL-induced reactive species (RS) production and reduced glutathione (GSH) depletion. Moreover, DD (1 ฮผM) per se improved the maximal mitochondrial respiratory capacity and prevented oxLDL-induced mitochondrial damage. In addition, DD could prevent apoptosis induced by oxLDL in BAEC. Results from this study may provide insight into a possible molecular mechanism underlying DD suppression of oxLDL-mediated vascular endothelial dysfunction. | ||
|keywords=Bovine aortic endothelial cells | |keywords=Bovine aortic endothelial cells | ||
|mipnetlab=BR Rio de Janeiro Rumjanek FD, BR Rio de Janeiro Galina A | |mipnetlab=BR Rio de Janeiro Rumjanek FD, BR Rio de Janeiro Galina A | ||
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{{Labeling | {{Labeling | ||
Revision as of 14:26, 22 August 2014
| Hort MA, Straliotto MR, de Oliveira J, Amoรชdo ND, da Rocha JB, Galina A, Ribeiro-do-Valle RM, de Bem AF (2014) Diphenyl diselenide protects endothelial cells against oxidized low density lipoprotein-induced injury: Involvement of mitochondrial function. Biochimie [Epub ahead of print]. |
Hort MA, Straliotto MR, de Oliveira J, Amoedo ND, da Rocha JB, Galina A, Ribeiro-do-Valle RM, de Bem AF (2014) Biochimie
Abstract: Elevated levels of oxidized low density lipoprotein (oxLDL) are considered to be one of the major risk factors for atherosclerosis and cardiovascular morbidity. The early stages of atherosclerosis are initiated by the accumulation of oxLDL and the induction of toxic effects on endothelial cells, resulting in endothelial dysfunction. The aim of this study was to investigate how diphenyl diselenide (DD), an organoselenium compound, protect vascular endothelial cells against the toxic effects of oxLDL in vitro. Our data showed that the treatment of bovine endothelial aortic cells (BAEC) with DD (0.1-1 ฮผM) for 24 h protected from oxLDL-induced reactive species (RS) production and reduced glutathione (GSH) depletion. Moreover, DD (1 ฮผM) per se improved the maximal mitochondrial respiratory capacity and prevented oxLDL-induced mitochondrial damage. In addition, DD could prevent apoptosis induced by oxLDL in BAEC. Results from this study may provide insight into a possible molecular mechanism underlying DD suppression of oxLDL-mediated vascular endothelial dysfunction. โข Keywords: Bovine aortic endothelial cells
โข O2k-Network Lab: BR Rio de Janeiro Rumjanek FD, BR Rio de Janeiro Galina A
Labels: MiParea: Respiration, Pharmacology;toxicology
Organism: Bovines
Preparation: Intact cells
Coupling state: LEAK, ROUTINE, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property.
HRR: Oxygraph-2k
