Difference between revisions of "Makrecka-Kuka 2016 Abstract MitoFit Science Camp 2016"
Beno Marija (talk | contribs) |
|||
| (2 intermediate revisions by one other user not shown) | |||
| Line 1: | Line 1: | ||
{{Abstract | {{Abstract | ||
|title=Long-chain acylCoAs vs acylcarnitines in mitochondrial bioenergetics: from ''in vitro'' to ''in vivo''. | |||
|authors=Makrecka-Kuka M, Kuka J, Volska K, Makarova E, Sevostjanovs E, Dambrova M, Liepinsh E | |||
|year=2016 | |year=2016 | ||
|event=MitoFit Science Camp 2016 Kuehtai AT | |event=MitoFit Science Camp 2016 Kuehtai AT | ||
|abstract=Fatty acid metabolism plays an essential role in muscles bioenergetics. The accumulation of long-chain fatty acids and their activated intermediates, CoA and carnitine esters, is observed in the ischemic myocardium after acute ischemia-reperfusion. The aim of the study was to compare long-chain acyl-CoAs and acylcarnitine effects on mitochondrial bioenergetics and identify harmful fatty acid intermediates. | |||
The acute effects of palmitoyl-CoA and palmitoylcarnitine were studied in isolated rat cardiac mitochondria. To study the effects ''in vivo'', pharmacological regulation of the availability of activated fatty acids by meldonium and methyl-GBB were used. | |||
Palmitoylcarnitine, but not palmitoyl-CoA, was able to significantly reduce the pyruvate oxidation rate in mitochondria. Both palmitoyl-CoA and palmitoylcarnitine decreased OXPHOS-dependent mitochondrial respiration in dose-dependent manner. Despite that palmitoyl-CoA is approximately 2.5 times more toxic than palmitoylcarnitine, cardiac mitochondria are better protected against acyl-CoAs than against acylcarnitines due to protection by acyl-CoA-binding protein. Moreover, in ischemic mitochondria the content of long-chain acyl-CoAs was up to 50-fold lower than the measured acylcarnitine content. The pharmacological reduction of long-chain acylcarnitine content in mitochondria decreases ischemia-reperfusion induced mitochondrial dysfunction and significantly decreases infarct size. | |||
Overall, present results demonstrate that long-chain acylcarnitines, but not long-chain acyl-CoAs, orchestrate mitochondrial energy metabolism pattern and determine ischemia-reperfusion induced damage in cardiac mitochondria. | |||
|mipnetlab=LV Riga Makrecka-Kuka M | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=mt-Biogenesis;mt-density | |||
|organism=Rat | |||
|tissues=Heart | |||
|preparations=Isolated mitochondria | |||
|injuries=Ischemia-reperfusion | |||
|couplingstates=OXPHOS | |||
|pathways=F | |||
|event=A1 | |event=A1 | ||
|additional=MitoFit Science Camp 2016 | |additional=MitoFit Science Camp 2016 | ||
}} | }} | ||
== Affiliations == | == Affiliations == | ||
1-Latvian Inst Organic Synthesis, Lab Pharmaceutical Pharmacol; 2-Riga Stradins Univ, Fac Pharmacy, Riga, Latvia. - makrecka@farm.osi.lv | |||
Latest revision as of 11:26, 8 November 2016
| Long-chain acylCoAs vs acylcarnitines in mitochondrial bioenergetics: from in vitro to in vivo. |
Link:
Makrecka-Kuka M, Kuka J, Volska K, Makarova E, Sevostjanovs E, Dambrova M, Liepinsh E (2016)
Event: MitoFit Science Camp 2016 Kuehtai AT
Fatty acid metabolism plays an essential role in muscles bioenergetics. The accumulation of long-chain fatty acids and their activated intermediates, CoA and carnitine esters, is observed in the ischemic myocardium after acute ischemia-reperfusion. The aim of the study was to compare long-chain acyl-CoAs and acylcarnitine effects on mitochondrial bioenergetics and identify harmful fatty acid intermediates.
The acute effects of palmitoyl-CoA and palmitoylcarnitine were studied in isolated rat cardiac mitochondria. To study the effects in vivo, pharmacological regulation of the availability of activated fatty acids by meldonium and methyl-GBB were used.
Palmitoylcarnitine, but not palmitoyl-CoA, was able to significantly reduce the pyruvate oxidation rate in mitochondria. Both palmitoyl-CoA and palmitoylcarnitine decreased OXPHOS-dependent mitochondrial respiration in dose-dependent manner. Despite that palmitoyl-CoA is approximately 2.5 times more toxic than palmitoylcarnitine, cardiac mitochondria are better protected against acyl-CoAs than against acylcarnitines due to protection by acyl-CoA-binding protein. Moreover, in ischemic mitochondria the content of long-chain acyl-CoAs was up to 50-fold lower than the measured acylcarnitine content. The pharmacological reduction of long-chain acylcarnitine content in mitochondria decreases ischemia-reperfusion induced mitochondrial dysfunction and significantly decreases infarct size.
Overall, present results demonstrate that long-chain acylcarnitines, but not long-chain acyl-CoAs, orchestrate mitochondrial energy metabolism pattern and determine ischemia-reperfusion induced damage in cardiac mitochondria.
• O2k-Network Lab: LV Riga Makrecka-Kuka M
Labels: MiParea: mt-Biogenesis;mt-density
Stress:Ischemia-reperfusion Organism: Rat Tissue;cell: Heart Preparation: Isolated mitochondria
Coupling state: OXPHOS
Pathway: F
Event: A1 MitoFit Science Camp 2016
Affiliations
1-Latvian Inst Organic Synthesis, Lab Pharmaceutical Pharmacol; 2-Riga Stradins Univ, Fac Pharmacy, Riga, Latvia. - makrecka@farm.osi.lv
