Mitochondria as sources and targets of methane

András Tamás Mészáros, ágnes Lilla Szilágyi, László Juhász, Eszter Tuboly, Dániel érces, Gabriella Varga, P. Hartmann

Research output: Contribution to journalShort survey

4 Citations (Scopus)

Abstract

This review summarizes the current knowledge on the role of mitochondria in the context of hypoxic cell biology, while providing evidence of how these mechanisms are modulated by methane (CH 4 ). Recent studies have unambiguously confirmed CH 4 bioactivity in various in vitro and in vivo experimental models and established the possibility that CH 4 can affect many aspects of mitochondrial physiology. To date, no specific binding of CH 4 to any enzymes or receptors have been reported, and it is probable that many of its effects are related to physico-chemical properties of the non-polar molecule. (i) Mitochondria themselves can be sources of endogenous CH 4 generation under oxido-reductive stress conditions; chemical inhibition of the mitochondrial electron transport chain with site-specific inhibitors leads to increased formation of CH 4 in eukaryote cells, in plants, and in animals. (ii) Conventionally believed as physiologically inert, studies cited in this review demonstrate that exogenous CH 4 modulates key events of inflammation. The anti-apoptotic effects of exogenously administered CH 4 are also recognized, and these properties also suggest that CH 4 -mediated intracellular signaling is closely associated with mitochondria. (iii) Mitochondrial substrate oxidation is coupled with the reduction of molecular oxygen, thus providing energy for cellular metabolism. Interestingly, recent in vivo studies have shown improved basal respiration and modulated mitochondrial oxidative phosphorylation by exogenous CH 4 . Overall, these data suggest that CH 4 liberation and effectiveness in eukaryotes are both linked to hypoxic events and redox regulation and support the notion that CH 4 has therapeutic roles in mammalian pathophysiologies.

Original languageEnglish
Article number00195
JournalFrontiers in Medicine
Volume4
Issue numberNOV
DOIs
Publication statusPublished - Jan 1 2017

Fingerprint

Methane
Mitochondria
Eukaryota
Oxidative Phosphorylation
Plant Cells
Electron Transport
Energy Metabolism
Oxidation-Reduction
Cell Biology
Respiration
Theoretical Models
Oxygen
Inflammation
Enzymes
Therapeutics

Keywords

  • Apoptosis
  • Gasotransmitter
  • Methane
  • Mitochondrion
  • Review

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Mészáros, A. T., Szilágyi, Á. L., Juhász, L., Tuboly, E., érces, D., Varga, G., & Hartmann, P. (2017). Mitochondria as sources and targets of methane. Frontiers in Medicine, 4(NOV), [00195]. https://doi.org/10.3389/fmed.2017.00195

Mitochondria as sources and targets of methane. / Mészáros, András Tamás; Szilágyi, ágnes Lilla; Juhász, László; Tuboly, Eszter; érces, Dániel; Varga, Gabriella; Hartmann, P.

In: Frontiers in Medicine, Vol. 4, No. NOV, 00195, 01.01.2017.

Research output: Contribution to journalShort survey

Mészáros, AT, Szilágyi, ÁL, Juhász, L, Tuboly, E, érces, D, Varga, G & Hartmann, P 2017, 'Mitochondria as sources and targets of methane', Frontiers in Medicine, vol. 4, no. NOV, 00195. https://doi.org/10.3389/fmed.2017.00195
Mészáros AT, Szilágyi ÁL, Juhász L, Tuboly E, érces D, Varga G et al. Mitochondria as sources and targets of methane. Frontiers in Medicine. 2017 Jan 1;4(NOV). 00195. https://doi.org/10.3389/fmed.2017.00195
Mészáros, András Tamás ; Szilágyi, ágnes Lilla ; Juhász, László ; Tuboly, Eszter ; érces, Dániel ; Varga, Gabriella ; Hartmann, P. / Mitochondria as sources and targets of methane. In: Frontiers in Medicine. 2017 ; Vol. 4, No. NOV.
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