Mitochondria As Sources and Targets of Methane

Mészáros, András; Szilágyi, Ágnes Lilla; Juhász, László; Tuboly, Eszter; Érces, Dániel; Varga, Gabriella; Hartmann, Petra

doi:10.3389/fmed.2017.00195

Cited by 19 publications

(16 citation statements)

References 64 publications

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“…A key mechanism of IRI is associated with excessive oxidative stress, in which the mitochondrial respiratory chain is the main source of destructive reactive oxygen species (ROS) [18]. Previous reports have found that CH4-mediated intracellular signaling is closely related to mitochondria [19]. Sirt3 is a NAD+-dependent protein deacetylase that is exclusively localized in the mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Methane-Rich Saline: A Potential Resuscitation Fluid for Hemorrhagic Shock

Tong

Dong

Yang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Hemorrhagic shock is caused by massive blood loss. If the patient is not fully resuscitated in time, this may eventually lead to multiple organ failure and even death. Previous studies on methane-rich saline in animal models showed that it confers resistance against many diseases. In this study, we explored the protective effect of methane-rich saline, used as a resuscitation fluid, in hemorrhagic shock. Hemorrhagic shock was induced in SD rats by bloodletting via intubation of the right femoral artery. The rats were divided into three groups: a sham control group (sham control), a shock group resuscitated by an infusion of autologous blood and an equivalent volume of normal saline (Shock+NS), and a shock group resuscitated by an infusion of autologous blood and an equivalent volume of methane-rich saline (Shock+MRS). Assessment of blood pressure and levels of plasma lactate showed that resuscitation using methane-rich saline (MRS) restored systemic blood pressure and reduced the levels of lactate in the plasma. Meanwhile, lower levels of serum IL-6 and TNF-α were also observed in the group resuscitated with MRS. In the heart, liver, and kidney, MRS reduced inflammation and oxidative stress levels. Analysis of organ function via levels of biochemical indicators revealed that the group resuscitated with MRS had reduced serum levels of AST and CK, indicating a potential cardioprotective effect. The expression levels of apoptosis-related proteins, including those of Bcl-2/Bax, and the results of TUNEL-labeling assay indicated that MRS significantly reduced apoptosis in the heart. Methane also had a positive effect on the expression of the PGC-1α/SIRT3/SOD2 signaling pathway. Our results showed that MRS can potentially serve as a novel resuscitation fluid because of its anti-inflammatory, antioxidative, and antiapoptotic properties.

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Section: Discussionmentioning

confidence: 99%

Methane-Rich Saline: A Potential Resuscitation Fluid for Hemorrhagic Shock

Tong

Dong

Yang

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…Lastly, it seems that mitochondria may have a fundamental role to connect the individual effects of distinct interventions, providing an explanation of why CH 4 supplementation may interfere with the consequences of diverse conditions associated with hypoxia and inflammation (Mészáros et al, 2017b). It is well established that the antigen-independent IR stimulus can initiate mitochondria-related intrinsic signaling pathways of apoptosis.…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Methane Production and Bioactivity-A Link to Oxido-Reductive Stress

Boros

Keppler

2019

Front. Physiol.

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Biological methane formation is associated with anoxic environments and the activity of anaerobic prokaryotes (Archaea). However, recent studies have confirmed methane release from eukaryotes, including plants, fungi, and animals, even in the absence of microbes and in the presence of oxygen. Furthermore, it was found that aerobic methane emission in plants is stimulated by a variety of environmental stress factors, leading to reactive oxygen species (ROS) generation. Further research presented evidence that molecules with sulfur and nitrogen bonded methyl groups such as methionine or choline are carbon precursors of aerobic methane formation. Once generated, methane is widely considered to be physiologically inert in eukaryotes, but several studies have found association between mammalian methanogenesis and gastrointestinal (GI) motility changes. In addition, a number of recent reports demonstrated anti-inflammatory potential for exogenous methane-based approaches in model anoxia-reoxygenation experiments. It has also been convincingly demonstrated that methane can influence the downstream effectors of transiently increased ROS levels, including mitochondria-related pro-apoptotic pathways during ischemia-reperfusion (IR) conditions. Besides, exogenous methane can modify the outcome of gasotransmitter-mediated events in plants, and it appears that similar mechanism might be active in mammals as well. This review summarizes the relevant literature on methane-producing processes in eukaryotes, and the available results that underscore its bioactivity. The current evidences suggest that methane liberation and biological effectiveness are both linked to cellular redox regulation. The data collectively imply that exogenous methane influences the regulatory mechanisms and signaling pathways involved in oxidative and nitrosative stress responses, which suggests a modulator role for methane in hypoxia-linked pathologies.

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“…Strifler et al have showed that methane can improve mitochondrial respiration [22]. Meszaros et al demonstrated that mitochondria are targets of methane [23]. Considering this characteristic, we hypothesize that MRS can inhibit inflammation and mitochondrial damage-induced pyroptosis to protect against liver damage in a cholestatic rat model.…”

Section: Discussionmentioning

confidence: 75%

Methane-Rich Saline Counteracts Cholestasis-Induced Liver Damage via Regulating the TLR4/NF-κB/NLRP3 Inflammasome Pathway

Chen

Jia

et al. 2019

Oxidative Medicine and Cellular Longevity

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Cholestatic liver injury, due to obstruction of the biliary tract or genetic defects, is often accompanied by progressive inflammation and liver fibrosis. Methane-rich saline (MRS) has anti-inflammatory properties. However, whether MRS can provide protective effect in cholestatic liver injury is still unclear. In this study, Sprague-Dawley rats received bile duct ligation (BDL) to generate a cholestatic model followed by MRS treatment (10 mL/kg, ip treatment) every 12 h after the operation to explore the potential protective mechanism of MRS in cholestatic liver injury. We found that MRS effectively improved liver function, alleviated liver pathological damage, and localized infiltration of inflammatory cells. MRS treatment decreased the expression of hepatic fibrosis-associated proteins to alleviate liver fibrosis. Furthermore, MRS treatment suppressed the TLR4/NF-κB pathway and further reduced the levels of proinflammatory factors. Downregulation of NF-κB subsequently reduced the NLRP3 expression to inhibit pyroptosis. Our data indicated that methane treatment prevented cholestatic liver injury via anti-inflammatory properties that involved the TLR4/NF-κB/NLRP3 signaling pathway.

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Mitochondria As Sources and Targets of Methane

Cited by 19 publications

References 64 publications

Methane-Rich Saline: A Potential Resuscitation Fluid for Hemorrhagic Shock

Methane-Rich Saline: A Potential Resuscitation Fluid for Hemorrhagic Shock

Methane Production and Bioactivity-A Link to Oxido-Reductive Stress

Methane-Rich Saline Counteracts Cholestasis-Induced Liver Damage via Regulating the TLR4/NF-κB/NLRP3 Inflammasome Pathway

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