Difference between revisions of "Labieniec 2009 Chem Biol Interact"
| Line 5: | Line 5: | ||
|journal=Chem. Biol. Interact. | |journal=Chem. Biol. Interact. | ||
|abstract=In the present investigation, we attempted to study possible mechanisms of the interactions of resorcylidene aminoguanidine (RAG), the agent with a recognized anti-glycation and antioxidative activity, with rat liver mitochondria. We hypothesized that RAG affects organization of the lipid bilayer in mitochondrial membranes and thus impairs transmembrane Ca<sup>2+</sup> redistribution, transmembrane potential, and respiration capacity. Isolated mitochondria were exposed to RAG (50–200 μM) and several parameters of their function monitored employing spectrofluorimetric, cytometric, and respirometric techniques. Mitochondrial membrane potential and membrane fluidity were tracked using the staining with rhodamine 123 (Rh123) and 1,6-diphenyl-1,3,5-hexatriene (DPH), respectively. Mitochondrial respiration and oxidative phosphorylation was monitored with a high-resolution respirometry, and mobilization of Ca<sup>2+</sup> was detected using spectrofluorimetry with Calcium Green 5-N. RAG depolarized and fluidized mitochondrial membrane, as deduced from reduced fluorescence of intramitochondrial Rh123 and decreased DPH fluorescence anisotropy. The slight inhibitory effect of 100–200 μM RAG on mitochondrial respiratory capacity was observed merely when monitored in the presence of ADP. The reduced sensitivity of mitochondria to calcium-induced depolarization was significant only at higher RAG concentrations (100–200 μM). Moreover, RAG induced pronounced conformational changes in two model proteins: bovine serum albumin and cytochrome ''c''. These findings indicate that regardless of its depolarizing and fluidizing properties, RAG does not largely affect the mitochondrial respiration, although it may significantly lower oxidative phosphorylation when used at higher concentrations. | |abstract=In the present investigation, we attempted to study possible mechanisms of the interactions of resorcylidene aminoguanidine (RAG), the agent with a recognized anti-glycation and antioxidative activity, with rat liver mitochondria. We hypothesized that RAG affects organization of the lipid bilayer in mitochondrial membranes and thus impairs transmembrane Ca<sup>2+</sup> redistribution, transmembrane potential, and respiration capacity. Isolated mitochondria were exposed to RAG (50–200 μM) and several parameters of their function monitored employing spectrofluorimetric, cytometric, and respirometric techniques. Mitochondrial membrane potential and membrane fluidity were tracked using the staining with rhodamine 123 (Rh123) and 1,6-diphenyl-1,3,5-hexatriene (DPH), respectively. Mitochondrial respiration and oxidative phosphorylation was monitored with a high-resolution respirometry, and mobilization of Ca<sup>2+</sup> was detected using spectrofluorimetry with Calcium Green 5-N. RAG depolarized and fluidized mitochondrial membrane, as deduced from reduced fluorescence of intramitochondrial Rh123 and decreased DPH fluorescence anisotropy. The slight inhibitory effect of 100–200 μM RAG on mitochondrial respiratory capacity was observed merely when monitored in the presence of ADP. The reduced sensitivity of mitochondria to calcium-induced depolarization was significant only at higher RAG concentrations (100–200 μM). Moreover, RAG induced pronounced conformational changes in two model proteins: bovine serum albumin and cytochrome ''c''. These findings indicate that regardless of its depolarizing and fluidizing properties, RAG does not largely affect the mitochondrial respiration, although it may significantly lower oxidative phosphorylation when used at higher concentrations. | ||
|keywords= (bio)Membranes, Rat liver mitochondria, Resorcylidene aminoguanidine (RAG), Membrane potential, Ca<sup>2+</sup> homeostasis, Membrane fluidity | |keywords=(bio)Membranes, Rat liver mitochondria, Resorcylidene aminoguanidine (RAG), Membrane potential, Ca<sup>2+</sup> homeostasis, Membrane fluidity | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19061873 PMID: 19061873] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/19061873 PMID: 19061873] | ||
}} | }} | ||
| Line 17: | Line 17: | ||
|topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential, Ion Homeostasis | |topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential, Ion Homeostasis | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Revision as of 13:46, 18 October 2010
| Labieniec M, Przygodzki T, Cársky J, Malinska D, Rysz J, Watala C (2009) Effects of resorcylidene aminoguanidine (RAG) on selected parameters of isolated rat liver mitochondria. Chem. Biol. Interact. 179: 280-287. |
Labieniec M, Przygodzki T, Carsky J, Malinska D, Rysz J, Watala C (2009) Chem. Biol. Interact.
Abstract: In the present investigation, we attempted to study possible mechanisms of the interactions of resorcylidene aminoguanidine (RAG), the agent with a recognized anti-glycation and antioxidative activity, with rat liver mitochondria. We hypothesized that RAG affects organization of the lipid bilayer in mitochondrial membranes and thus impairs transmembrane Ca2+ redistribution, transmembrane potential, and respiration capacity. Isolated mitochondria were exposed to RAG (50–200 μM) and several parameters of their function monitored employing spectrofluorimetric, cytometric, and respirometric techniques. Mitochondrial membrane potential and membrane fluidity were tracked using the staining with rhodamine 123 (Rh123) and 1,6-diphenyl-1,3,5-hexatriene (DPH), respectively. Mitochondrial respiration and oxidative phosphorylation was monitored with a high-resolution respirometry, and mobilization of Ca2+ was detected using spectrofluorimetry with Calcium Green 5-N. RAG depolarized and fluidized mitochondrial membrane, as deduced from reduced fluorescence of intramitochondrial Rh123 and decreased DPH fluorescence anisotropy. The slight inhibitory effect of 100–200 μM RAG on mitochondrial respiratory capacity was observed merely when monitored in the presence of ADP. The reduced sensitivity of mitochondria to calcium-induced depolarization was significant only at higher RAG concentrations (100–200 μM). Moreover, RAG induced pronounced conformational changes in two model proteins: bovine serum albumin and cytochrome c. These findings indicate that regardless of its depolarizing and fluidizing properties, RAG does not largely affect the mitochondrial respiration, although it may significantly lower oxidative phosphorylation when used at higher concentrations. • Keywords: (bio)Membranes, Rat liver mitochondria, Resorcylidene aminoguanidine (RAG), Membrane potential, Ca2+ homeostasis, Membrane fluidity
Labels:
Stress:Genetic Defect; Knockdown; Overexpression"Genetic Defect; Knockdown; Overexpression" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Rat Tissue;cell: Hepatocyte; Liver"Hepatocyte; Liver" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property. Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Coupling; Membrane Potential"Coupling; Membrane Potential" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Ion Homeostasis"Ion Homeostasis" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k
