Volska 2018 MiP2018: Difference between revisions
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{{Abstract | {{Abstract | ||
|title=[[Image:MiPsocietyLOGO.JPG|left|90px|Mitochondrial Physiology Society|MiPsociety]] | |title=[[Image:MiPsocietyLOGO.JPG|left|90px|Mitochondrial Physiology Society|MiPsociety]] The mechanisms of long-chain acylcarnitine accumulation during ischemia. | ||
|info=[[MiP2018]] | |info=[[MiP2018]] | ||
|authors=Volska K, Liepinsh E, Makarova E, Makrecka-Kuka M, Kuka J, Dambrova M | |||
|year=2018 | |year=2018 | ||
|event=MiP2018 | |event=MiP2018 | ||
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]] | |abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoglobal.org/index.php/MITOEAGLE|COST Action MitoEAGLE]] | ||
The accumulation of long-chain acylcarnitines is observed in the ischemic myocardium and there is evidence that long-chain acylcarnitines determine the ischemia/reperfusion-induced damage in heart mitochondria. The aim of this study was to identify the mechanisms of long-chain acylcarnitine accumulation in the heart mitochondria during ischemia. | |||
To study long-chain acylcarnitine accumulation in mitochondrial fractions, labelled [3H]-palmitoyl-carnitine content was measured in the inner and outer mitochondrial membranes, intermembrane space and mitochondrial matrix. To clarify the possible mechanisms of long-chain acylcarnitine accumulation during ischemia, mitochondrial respiration with palmitoyl-CoA, the activity of carnitine palmitoyltransferase (CPT) 1, CPT2-dependent β-oxidation, concentrations of acyl-CoA and CoA were measured in mitochondria isolated from the non-risk area and the area at risk of ischemic hearts. | |||
Results indicated that the main locations of palmitoyl-carnitine accumulation are the inner mitochondrial membrane and the intermembrane space. Mitochondria isolated from area at risk had a 25% lower mitochondrial respiration rate with palmitoyl-CoA compared with those in non-risk area. The CPT1 activity in the area at risk was increased by 40%, whereas CPT2-dependent β-oxidation was decreased by 42% compared with the non-risk area. The ratio of acyl-CoA/CoA in the area at risk was almost 3-fold higher compared with that in the non-risk area, indicating that mitochondrial CoA pool is depleted. | |||
In conclusion, long-chain acylcarnitine accumulation in the mitochondrial intermembrane space is a result of increased CPT1 activity and decreased CPT2-dependent fatty acid metabolism in mitochondria of ischemic myocardium. | |||
|editor=[[Plangger M]], [[Kandolf G]] | |editor=[[Plangger M]], [[Kandolf G]] | ||
|mipnetlab=LV Riga Makrecka-Kuka M | |||
}} | |||
{{Labeling | |||
|area=Respiration | |||
|injuries=Ischemia-reperfusion | |||
|tissues=Heart | |||
|preparations=Isolated mitochondria | |||
|topics=Fatty acid | |||
|instruments=Oxygraph-2k | |||
}} | }} | ||
== Affiliations == | == Affiliations == | ||
Volska K(1,2), Liepinsh E(1), Makarova E(1), Makrecka-Kuka M(1), Kuka J(1), Dambrova M(1,2) | |||
::::#Latvian Inst Organic Synthesis | |||
::::#Riga Stradins Univ, Fac Pharmacy; Riga, Latvia |
Revision as of 12:09, 27 August 2018
The mechanisms of long-chain acylcarnitine accumulation during ischemia. |
Link: MiP2018
Volska K, Liepinsh E, Makarova E, Makrecka-Kuka M, Kuka J, Dambrova M (2018)
Event: MiP2018
The accumulation of long-chain acylcarnitines is observed in the ischemic myocardium and there is evidence that long-chain acylcarnitines determine the ischemia/reperfusion-induced damage in heart mitochondria. The aim of this study was to identify the mechanisms of long-chain acylcarnitine accumulation in the heart mitochondria during ischemia.
To study long-chain acylcarnitine accumulation in mitochondrial fractions, labelled [3H]-palmitoyl-carnitine content was measured in the inner and outer mitochondrial membranes, intermembrane space and mitochondrial matrix. To clarify the possible mechanisms of long-chain acylcarnitine accumulation during ischemia, mitochondrial respiration with palmitoyl-CoA, the activity of carnitine palmitoyltransferase (CPT) 1, CPT2-dependent β-oxidation, concentrations of acyl-CoA and CoA were measured in mitochondria isolated from the non-risk area and the area at risk of ischemic hearts.
Results indicated that the main locations of palmitoyl-carnitine accumulation are the inner mitochondrial membrane and the intermembrane space. Mitochondria isolated from area at risk had a 25% lower mitochondrial respiration rate with palmitoyl-CoA compared with those in non-risk area. The CPT1 activity in the area at risk was increased by 40%, whereas CPT2-dependent β-oxidation was decreased by 42% compared with the non-risk area. The ratio of acyl-CoA/CoA in the area at risk was almost 3-fold higher compared with that in the non-risk area, indicating that mitochondrial CoA pool is depleted.
In conclusion, long-chain acylcarnitine accumulation in the mitochondrial intermembrane space is a result of increased CPT1 activity and decreased CPT2-dependent fatty acid metabolism in mitochondria of ischemic myocardium.
• Bioblast editor: Plangger M, Kandolf G
• O2k-Network Lab: LV Riga Makrecka-Kuka M
Labels: MiParea: Respiration
Stress:Ischemia-reperfusion
Tissue;cell: Heart Preparation: Isolated mitochondria
Regulation: Fatty acid
HRR: Oxygraph-2k
Affiliations
Volska K(1,2), Liepinsh E(1), Makarova E(1), Makrecka-Kuka M(1), Kuka J(1), Dambrova M(1,2)
- Latvian Inst Organic Synthesis
- Riga Stradins Univ, Fac Pharmacy; Riga, Latvia