Reduction in hypoxia‐reoxygenation‐induced myocardial mitochondrial damage with exogenous methane

Jász, Dávid Kurszán; Szilágyi, Ágnes Lilla; Tuboly, Eszter; Baráth, Bálint; Márton, Anett Roxána; Varga, Pál S.; Varga, Gabriella; Érces, Dániel; Mohácsi, Árpád; Szabó, Anna; Bozó, Renáta; Gömöri, Kamilla; Görbe, Anikó; Boros, Mihály; Hartmann, Petra

doi:10.1111/jcmm.16498

Cited by 6 publications

(6 citation statements)

References 39 publications

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“…Furthermore, our data suggested intracellular ROS played a critical role, since both antioxidant and ROS scavenger reduced ROS ( Figure 3 ) and abolished hypoxia-induced mitochondrial malfunction ( Figure 3 ). The pivotal role of ROS during hypoxia-induced mitochondrial malfunction was also supported by previous publications, which demonstrated that hypoxia may impair mitochondrial function through inducing oxidative stress in rat cardiomyocytes [ 28 ], human renal tubular cells [ 29 ], murine fibroblasts [ 30 ], rat cerebral neuronal glial cells [ 31 ], and primary rat hippocampal neurons [ 32 ].…”

Section: Discussionsupporting

confidence: 56%

Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons

Han

Tao

Cui

et al. 2022

Oxidative Medicine and Cellular Longevity

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Background. Hypoxia may induce mitochondrial abnormality, which is associated with a variety of clinical phenotypes in the central nervous system. Propofol is an anesthetic agent with neuroprotective property. We examined whether and how propofol protected hypoxia-induced mitochondrial abnormality in neurons. Methods. Primary rat hippocampal neurons were exposed to propofol followed by hypoxia treatment. Neuron viability, mitochondrial morphology, mitochondrial permeability transition pore (mPTP) opening, mitochondrial membrane potential (MMP), and adenosine triphosphate (ATP) production were measured. Mechanisms including reactive oxygen species (ROS), extracellular regulated protein kinase (ERK), protein kinase A (PKA), HIF-1α, Drp1, Fis1, Mfn1, Mfn2, and Opa1 were investigated. Results. Hypoxia increased intracellular ROS production and induced mPTP opening, while reducing ATP production, MMP values, and neuron viability. Hypoxia impaired mitochondrial dynamic balance by increasing mitochondrial fragmentation. Further, hypoxia induced the translocation of HIF-1α and increased the expression of Drp1, while having no effect on Fis1 expression. In addition, hypoxia induced the phosphorylation of ERK and Drp1ser616, while reducing the phosphorylation of PKA and Drp1ser637. Importantly, we demonstrated all these effects were attenuated by pretreatment of neurons with 50 μM propofol, antioxidant α-tocopherol, and ROS scavenger ebselen. Besides, hypoxia, propofol, α-tocopherol, or ebselen had no effect on the expression of Mfn1, Mfn2, and Opa1. Conclusions. In rat hippocampal neurons, hypoxia induced oxidative stress, caused mitochondrial dynamic imbalance and malfunction, and reduced neuron viability. Propofol protected mitochondrial abnormality and neuron viability via antioxidant property, and the molecular mechanisms involved HIF-1α-mediated Drp1 expression and ERK/PKA-mediated Drp1 phosphorylation.

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Section: Discussionsupporting

confidence: 56%

Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons

Han

Tao

Cui

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Growing evidence indicates that mitochondrial function is impaired after acute A/R injury. MMP serves as a mitochondrial function marker, and MMP loss suggests abnormal mitochondrial function [ 35 ]. Figures 3(a) and 3(b) depict the significant MMP loss in the A/R group.…”

Section: Resultsmentioning

confidence: 99%

Ginsenoside Rg1 Ameliorates Acute Renal Ischemia/Reperfusion Injury via Upregulating AMPKα1 Expression

Zhou

Zhao

et al. 2022

Oxidative Medicine and Cellular Longevity

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Acute renal ischemia/reperfusion (I/R) injury often occurs during kidney transplantation and other kidney surgeries, and the molecular mechanism involves oxidative stress. We hypothesized that ginsenoside Rg1 (Rg1), a saponin derived from ginseng, would protect the renal tissue against acute renal I/R injury by upregulating 5 ′ adenosine monophosphate-activated protein kinase α1 (AMPKα1) expression and inhibiting oxidative stress. The models of acute anoxia/reoxygenation (A/R) damage in normal rat kidney epithelial cell lines (NRK-52E) and acute renal I/R injury in mice were constructed. The results revealed that pretreatment with 25 μM Rg1 significantly increased NRK-52E viability, decreased lactate dehydrogenase (LDH) activity and apoptosis, suppressed reactive oxygen species generation and oxidative stress, stabilized mitochondrial membrane potential and reduced mitochondria permeability transition pore openness, decreased adenosine monophosphate/adenosine triphosphate ratio, and upregulated the expression of AMPKα1, cytochrome b-c1 complex subunit 2, NADH dehydrogenase (ubiquinone) 1 beta subcomplex subunit 8, and B-cell lymphoma 2, while downregulating BCL2-associated X protein expression. The effects of Rg1 pretreatment were similar to those of pAD/Flag-AMPKα1. After acute renal I/R injury, serum creatinine, blood urea nitrogen, LDH activity, and oxidative stress in renal tissue significantly increased. Rg1 pretreatment upregulated AMPKα1 expression, which protects against acute renal I/R injury by maintaining renal function homeostasis, inhibiting oxidative stress, and reducing apoptosis. Compound C, a specific inhibitor of AMPK, reversed the effects of Rg1. In summary, Rg1 pretreatment upregulated AMPKα1 expression, inhibited oxidative stress, maintained mitochondrial function, improved energy metabolism, reduced apoptosis, and ultimately protected renal tissue against acute renal I/R injury.

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“…Inhaled CH 4 reduced cytochrome c release and preserved the mitochondrial respiratory capacity in vivo and in transient anoxia-treated cell cultures as well (Strifler et al, 2016;Jász et al, 2021). Recently, we carried out a sequential study with exogenous normoxic CH 4 in simulated IR environments using a high-resolution respirometry system to quantify the ETS responses (Jász et al, 2021). In this protocol, CH 4 treatment restricted the forward electron transfer within Complex I in control mitochondria while effectively restricting RET in postanoxic mitochondria, thus it could be concluded that interaction with Complex I occupies a key position in the protective mechanism of CH 4 against a hypoxia/reoxygenation injury (Jász et al, 2021).…”

Section: Inhaled Chmentioning

confidence: 96%

“…In this line, many studies have also explored the relationship among CH 4 actions in the context of mitochondrial biology. Inhaled CH 4 reduced cytochrome c release and preserved the mitochondrial respiratory capacity in vivo and in transient anoxia-treated cell cultures as well (Strifler et al, 2016;Jász et al, 2021). Recently, we carried out a sequential study with exogenous normoxic CH 4 in simulated IR environments using a high-resolution respirometry system to quantify the ETS responses (Jász et al, 2021).…”

Section: Inhaled Chmentioning

confidence: 99%

“…Recently, we carried out a sequential study with exogenous normoxic CH 4 in simulated IR environments using a high-resolution respirometry system to quantify the ETS responses (Jász et al, 2021). In this protocol, CH 4 treatment restricted the forward electron transfer within Complex I in control mitochondria while effectively restricting RET in postanoxic mitochondria, thus it could be concluded that interaction with Complex I occupies a key position in the protective mechanism of CH 4 against a hypoxia/reoxygenation injury (Jász et al, 2021). Parallel in vivo studies have also shown that the CH 4 content of an organ preservation solution effectively influenced several components of the endoplasmic reticulum (ER) stress-mitochondria-related pro-apoptotic signalling pathways (Benke et al, 2021).…”

Section: Inhaled Chmentioning

confidence: 99%

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Bioactivity of Inhaled Methane and Interactions With Other Biological Gases

Juhász

Tallósy

Nászai

et al. 2022

Front. Cell Dev. Biol.

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A number of studies have demonstrated explicit bioactivity for exogenous methane (CH4), even though it is conventionally considered as physiologically inert. Other reports cited in this review have demonstrated that inhaled, normoxic air-CH4 mixtures can modulate the in vivo pathways involved in oxidative and nitrosative stress responses and key events of mitochondrial respiration and apoptosis. The overview is divided into two parts, the first being devoted to a brief review of the effects of biologically important gases in the context of hypoxia, while the second part deals with CH4 bioactivity. Finally, the consequence of exogenous, normoxic CH4 administration is discussed under experimental hypoxia- or ischaemia-linked conditions and in interactions between CH4 and other biological gases, with a special emphasis on its versatile effects demonstrated in pulmonary pathologies.

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Reduction in hypoxia‐reoxygenation‐induced myocardial mitochondrial damage with exogenous methane

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 6 publications

References 39 publications

Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons

Propofol via Antioxidant Property Attenuated Hypoxia-Mediated Mitochondrial Dynamic Imbalance and Malfunction in Primary Rat Hippocampal Neurons

Ginsenoside Rg1 Ameliorates Acute Renal Ischemia/Reperfusion Injury via Upregulating AMPKα1 Expression

Bioactivity of Inhaled Methane and Interactions With Other Biological Gases

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