Difference between revisions of "Volska 2018 MiP2018"

From Bioblast
Jump to navigation Jump to search
 
Line 1: Line 1:
{{Abstract
{{Abstract
|title=[[Image:MiPsocietyLOGO.JPG|left|90px|Mitochondrial Physiology Society|MiPsociety]] The mechanisms of long-chain acylcarnitine accumulation during ischemia.
|title=[[Image:Volska K.JPG|left|90px|Kristina Volska]] 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
|authors=Volska K, Liepinsh E, Makarova E, Makrecka-Kuka M, Kuka J, Dambrova M
Line 8: Line 8:
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.
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.
To study long-chain acylcarnitine accumulation in mitochondrial fractions, labelled [<sup>3</sup>H]-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.
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.

Latest revision as of 12:16, 27 August 2018

Kristina Volska
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

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.


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)

  1. Latvian Inst Organic Synthesis
  2. Riga Stradins Univ, Fac Pharmacy; Riga, Latvia