Jasz 2021 J Cell Mol Med: Difference between revisions

Revision as of 14:30, 3 January 2023

Jász DK, Szilágyi ÁL, Tuboly E, Baráth B, Márton AR, Varga P, Varga G, Érces D, Mohácsi Á, Szabó A, Bozó R, Gömöri K, Görbe A, Boros M, Hartmann P (2021) Reduction in hypoxia-reoxygenation-induced myocardial mitochondrial damage with exogenous methane. https://doi.org/10.1111/jcmm.16498

» J Cell Mol Med 25:5113-23. PMID: 33942485 Open Access

Jasz David Kurszan, Szilagyi Agnes Lilla, Tuboly Eszter, Barath Balint, Marton Anett Roxana, Varga Petra, Varga Gabriella, Erces Daniel, Mohacsi Arpad, Szabo Anna, Bozo Renata, Goemoeri Kamilla, Goerbe Aniko, Boros Mihaly, Hartmann Petra (2021) J Cell Mol Med

Abstract: Albeit previous experiments suggest potential anti-inflammatory effect of exogenous methane (CH₄) in various organs, the mechanism of its bioactivity is not entirely understood. We aimed to investigate the potential mitochondrial effects and the underlying mechanisms of CH₄ in rat cardiomyocytes and mitochondria under simulated ischaemia/reperfusion (sI/R) conditions. Three-day-old cultured cardiomyocytes were treated with 2.2% CH₄ -artificial air mixture during 2-hour-long reoxygenation following 4-hour-long anoxia (sI/R and sI/R + CH₄ , n = 6-6), with normoxic groups serving as controls (SH and SH + CH₄ ; n = 6-6). Mitochondrial functions were investigated with high-resolution respirometry, and mitochondrial membrane injury was detected by cytochrome c release and apoptotic characteristics by using TUNEL staining. CH₄ admixture had no effect on complex II (CII)-linked respiration under normoxia but significantly decreased the complex I (CI)-linked oxygen consumption. Nevertheless, addition of CH₄ in the sI/R + CH₄ group significantly reduced the respiratory activity of CII in contrast to CI and the CH₄ treatment diminished mitochondrial H₂O₂ production. Substrate-induced changes to membrane potential were partially preserved by CH₄ , and additionally, cytochrome c release and apoptosis of cardiomyocytes were reduced in the CH₄ -treated group. In conclusion, the addition of CH₄ decreases mitochondrial ROS generation via blockade of electron transport at CI and reduces anoxia-reoxygenation-induced mitochondrial dysfunction and cardiomyocyte injury in vitro. • Keywords: Anoxia, Cardiomyocytes, Complex I, Methane, Mitochondrial membrane potential, Mitochondrial respiration, Reoxygenation • Bioblast editor: Plangger M

Labels: MiParea: Respiration, Pharmacology;toxicology

Stress:Ischemia-reperfusion Organism: Rat Tissue;cell: Heart

HRR: Oxygraph-2k

2023-01

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 |title=Jász DK, Szilágyi ÁL, Tuboly E, Baráth B, Márton AR, Varga P, Varga G, Érces D, Mohácsi Á, Szabó A, Bozó R, Gömöri K, Görbe A, Boros M, Hartmann P (2021) Reduction in hypoxia-reoxygenation-induced myocardial mitochondrial damage with exogenous methane. https://doi.org/10.1111/jcmm.16498
 |info=J Cell Mol Med 25:5113-23. [https://pubmed.ncbi.nlm.nih.gov/33942485 PMID: 33942485 Open Access]
-|authors=Jász DK, Szilágyi ÁL, Tuboly E, Baráth B, Márton AR, Varga P, Varga G, Érces D, Mohácsi Á, Szabó A, Bozó R, Gömöri K, Görbe A, Boros M, Hartmann P
+|authors=Jasz David Kurszan, Szilagyi Agnes Lilla, Tuboly Eszter, Barath Balint, Marton Anett Roxana, Varga Petra, Varga Gabriella, Erces Daniel, Mohacsi Arpad, Szabo Anna, Bozo Renata, Goemoeri Kamilla, Goerbe Aniko, Boros Mihaly, Hartmann Petra
 |year=2021
 |journal=J Cell Mol Med
-|abstract=Albeit previous experiments suggest potential anti-inflammatory effect of exogenous methane (CH4 ) in various organs, the mechanism of its bioactivity is not entirely understood. We aimed to investigate the potential mitochondrial effects and the underlying mechanisms of CH4 in rat cardiomyocytes and mitochondria under simulated ischaemia/reperfusion (sI/R) conditions. Three-day-old cultured cardiomyocytes were treated with 2.2% CH4 -artificial air mixture during 2-hour-long reoxygenation following 4-hour-long anoxia (sI/R and sI/R + CH4 , n = 6-6), with normoxic groups serving as controls (SH and SH + CH4 ; n = 6-6). Mitochondrial functions were investigated with high-resolution respirometry, and mitochondrial membrane injury was detected by cytochrome c release and apoptotic characteristics by using TUNEL staining. CH4 admixture had no effect on complex II (CII)-linked respiration under normoxia but significantly decreased the complex I (CI)-linked oxygen consumption. Nevertheless, addition of CH4 in the sI/R + CH4 group significantly reduced the respiratory activity of CII in contrast to CI and the CH4 treatment diminished mitochondrial H2 O2 production. Substrate-induced changes to membrane potential were partially preserved by CH4 , and additionally, cytochrome c release and apoptosis of cardiomyocytes were reduced in the CH4 -treated group. In conclusion, the addition of CH4 decreases mitochondrial ROS generation via blockade of electron transport at CI and reduces anoxia-reoxygenation-induced mitochondrial dysfunction and cardiomyocyte injury in vitro.
+|abstract=Albeit previous experiments suggest potential anti-inflammatory effect of exogenous methane (CH<sub>4</sub>) in various organs, the mechanism of its bioactivity is not entirely understood. We aimed to investigate the potential mitochondrial effects and the underlying mechanisms of CH<sub>4</sub> in rat cardiomyocytes and mitochondria under simulated ischaemia/reperfusion (sI/R) conditions. Three-day-old cultured cardiomyocytes were treated with 2.2% CH<sub>4</sub> -artificial air mixture during 2-hour-long reoxygenation following 4-hour-long anoxia (sI/R and sI/R + CH<sub>4</sub> , n = 6-6), with normoxic groups serving as controls (SH and SH + CH<sub>4</sub> ; n = 6-6). Mitochondrial functions were investigated with high-resolution respirometry, and mitochondrial membrane injury was detected by cytochrome c release and apoptotic characteristics by using TUNEL staining. CH<sub>4</sub> admixture had no effect on complex II (CII)-linked respiration under normoxia but significantly decreased the complex I (CI)-linked oxygen consumption. Nevertheless, addition of CH<sub>4</sub> in the sI/R + CH<sub>4</sub> group significantly reduced the respiratory activity of CII in contrast to CI and the CH<sub>4</sub> treatment diminished mitochondrial H<sub>2</sub>O<sub>2</sub> production. Substrate-induced changes to membrane potential were partially preserved by CH<sub>4</sub> , and additionally, cytochrome c release and apoptosis of cardiomyocytes were reduced in the CH<sub>4</sub> -treated group. In conclusion, the addition of CH<sub>4</sub> decreases mitochondrial ROS generation via blockade of electron transport at CI and reduces anoxia-reoxygenation-induced mitochondrial dysfunction and cardiomyocyte injury ''in vitro''.
 |keywords=Anoxia, Cardiomyocytes, Complex I, Methane, Mitochondrial membrane potential, Mitochondrial respiration, Reoxygenation
 |editor=[[Plangger M]]
 }}
 {{Labeling
-|area=Respiration
+|area=Respiration, Pharmacology;toxicology
+|injuries=Ischemia-reperfusion
+|organism=Rat
+|tissues=Heart
 |instruments=Oxygraph-2k
 |additional=2023-01
 }}