Abstract
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.
Highlights
IntroductionIn the Earth’s atmosphere, where oxygen (O2) accounts for ∼ 21% of the environmental gases, reduction-oxidation reactions provide the energy which makes complex organisms capable of sustaining life (Schmidt-Rohr, 2020)
Respiration From the Atmosphere to the CellsIn the Earth’s atmosphere, where oxygen (O2) accounts for ∼ 21% of the environmental gases, reduction-oxidation reactions provide the energy which makes complex organisms capable of sustaining life (Schmidt-Rohr, 2020)
The evolution of aerobic cells has created a range of control mechanisms for the optimal utilization of O2 for subcellular, mitochondrial respiration, where multiprotein complexes of the electron transport system (ETS) are dedicated to accepting electrons from reduced carriers and delivering them to accessible molecular O2
Summary
In the Earth’s atmosphere, where oxygen (O2) accounts for ∼ 21% of the environmental gases, reduction-oxidation reactions provide the energy which makes complex organisms capable of sustaining life (Schmidt-Rohr, 2020) Heterotrophs, such as humans, consume organic compounds for energy production by burning O2, with carbon dioxide (CO2) and water as the ultimate end products. The evolution of aerobic cells has created a range of control mechanisms for the optimal utilization of O2 for subcellular, mitochondrial respiration, where multiprotein complexes of the electron transport system (ETS) are dedicated to accepting electrons from reduced carriers and delivering them to accessible molecular O2. Three of these complexes (Complex I, III and IV) are H+ channels, responsible for a transmembrane electrochemical gradient between the surfaces of the inner membrane and the resulting driving force for ATP synthase (Complex V), which transforms adenosine diphosphate (ADP) into adenosine triphosphate (ATP)
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