Difference between revisions of "Sliwa 2012 Acta Biochim Pol"
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{{Publication | {{Publication | ||
|title=Sliwa A, | |title=Sliwa A, Goralska J, Czech U, Gruca A, Polus A, Zapala B, Dembinska-Kiec A (2012) Modulation of the human preadipocyte mitochondrial activity by beta-carotene. Acta Biochim Pol 59:39-41. | ||
|info= | |info=[http://www.actabp.pl/pdf/1_2012/39.pdf PMID: 22428124 Open Access] | ||
|authors=Sliwa A, Goralska J, Czech U, Gruca A, Polus A, Zapała B, Dembinska-Kiec A | |authors=Sliwa A, Goralska J, Czech U, Gruca A, Polus A, Zapała B, Dembinska-Kiec A | ||
|year=2012 | |year=2012 | ||
|journal=Acta Biochim Pol | |journal=Acta Biochim Pol | ||
|abstract=Increased ROS generation by the overload by metabolic substrates mitochondria paralleled by decrease of antioxidant activity are typical events found in metabolic syndrome and diabetes type 2. Metabolites of beta-carotene (BC) such as retinoic acid (RA), as well as low concentration of reactive oxygen species (ROS) modify the mitochondrial bioenergetic function. The aim of the study was to investigate the effect of beta-carotene on mitochondrial activity in human preadipocytes. BC used in concentrations, 10 or 30 µM, decreased mitochondrial membrane potential, inhibited mitochondrial respiration and decreased cellular ATP content. We conclude, that BC, the known antioxidant may decrease oxidative phosphorylation capacity of mitochondria. | |abstract=Increased ROS generation by the overload by metabolic substrates mitochondria paralleled by decrease of antioxidant activity are typical events found in metabolic syndrome and diabetes type 2. Metabolites of beta-carotene (BC) such as retinoic acid (RA), as well as low concentration of reactive oxygen species (ROS) modify the mitochondrial bioenergetic function. The aim of the study was to investigate the effect of beta-carotene on mitochondrial activity in human preadipocytes. BC used in concentrations, 10 or 30 µM, decreased mitochondrial membrane potential, inhibited mitochondrial respiration and decreased cellular ATP content. We conclude, that BC, the known antioxidant may decrease oxidative phosphorylation capacity of mitochondria. | ||
|keywords=Metabolic syndrome, diabetes | |keywords=Metabolic syndrome, diabetes, beta-carotene, retinoic acid, Chub-S7, preadipocytes | ||
|mipnetlab=PL Krakow Dembinska-Kiec A | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |||
|diseases=Diabetes | |||
|injuries=Oxidative stress;RONS | |||
|organism=Human | |||
|tissues=Fat | |||
|preparations=Intact cells | |||
|enzymes=Complex V;ATP synthase | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Latest revision as of 21:09, 18 March 2018
Sliwa A, Goralska J, Czech U, Gruca A, Polus A, Zapala B, Dembinska-Kiec A (2012) Modulation of the human preadipocyte mitochondrial activity by beta-carotene. Acta Biochim Pol 59:39-41. |
Sliwa A, Goralska J, Czech U, Gruca A, Polus A, Zapała B, Dembinska-Kiec A (2012) Acta Biochim Pol
Abstract: Increased ROS generation by the overload by metabolic substrates mitochondria paralleled by decrease of antioxidant activity are typical events found in metabolic syndrome and diabetes type 2. Metabolites of beta-carotene (BC) such as retinoic acid (RA), as well as low concentration of reactive oxygen species (ROS) modify the mitochondrial bioenergetic function. The aim of the study was to investigate the effect of beta-carotene on mitochondrial activity in human preadipocytes. BC used in concentrations, 10 or 30 µM, decreased mitochondrial membrane potential, inhibited mitochondrial respiration and decreased cellular ATP content. We conclude, that BC, the known antioxidant may decrease oxidative phosphorylation capacity of mitochondria. • Keywords: Metabolic syndrome, diabetes, beta-carotene, retinoic acid, Chub-S7, preadipocytes
• O2k-Network Lab: PL Krakow Dembinska-Kiec A
Labels: MiParea: Respiration
Pathology: Diabetes
Stress:Oxidative stress;RONS
Organism: Human
Tissue;cell: Fat
Preparation: Intact cells
Enzyme: Complex V;ATP synthase
HRR: Oxygraph-2k