Abstract
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.
Highlights
Methane (CH4) is a ubiquitous, intrinsically non-toxic gas. It is a simple asphyxiant, which means that CH4 will displace oxygen to approx. 18% in air when present at about 14% in a restricted area, but in this case hypoxia and the evolving cellular dysfunction will be due to the increasing concentration of CH4 and the decreased O2 content in the internal milieu and not to the chemical specificity of the gas (Boros et al, 2015)
Normoxic CH4 administration significantly decreased tissue nitric oxide (NO) levels in the hypoxic duodenal tissue already during the ischemic phase, which suggests that CH4 may directly modulate xanthine oxidoreductase (XOR) and XOR-linked nitrate reductase activities in the intestines (Poles et al, 2018). Another important aspect is that methane-enriched saline (MRS) decreased the expression levels of activated apoptosis signal-regulating kinase 1 (ASK-1), c-Jun NH2-terminal kinase (JNK) and the pro-apoptotic protein Bcl-2 associated X protein (Bax), and increased the expression of the anti-apoptotic proto-oncogene protein B cell leukemia/lymphoma-2 (Bcl2) proteins in a rat model of abdominal-island skin-flap IR (Song et al, 2015)
Similar results were demonstrated in several stress conditions coupled to redox imbalance which confirmed that Carbon monoxide (CO), NO, and H2S signaling mechanisms are involved in the molecular basis of CH4-induced stress tolerance in plant tissues (Han et al, 2017; Samma et al, 2017; Zhang et al, 2018)
Summary
Methane (CH4) is a ubiquitous, intrinsically non-toxic gas. It is a simple asphyxiant, which means that CH4 will displace oxygen to approx. 18% in air when present at about 14% (or 140000 parts per million by volume, ppmv) in a restricted area, but in this case hypoxia and the evolving cellular dysfunction will be due to the increasing concentration of CH4 and the decreased O2 content in the internal milieu and not to the chemical specificity of the gas (Boros et al, 2015).Methane BioactivityIn the Earth’s atmosphere, which contains approx. 1.8 ppmv CH4, a substantial part stems from the anaerobic degradation of biomass. Another important aspect is that methane-enriched saline (MRS) decreased the expression levels of activated apoptosis signal-regulating kinase 1 (ASK-1), c-Jun NH2-terminal kinase (JNK) and the pro-apoptotic protein Bcl-2 associated X protein (Bax), and increased the expression of the anti-apoptotic proto-oncogene protein B cell leukemia/lymphoma-2 (Bcl2) proteins in a rat model of abdominal-island skin-flap IR (Song et al, 2015).
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