Methane biogenesis during sodium azide-induced chemical hypoxia in rats

Eszter Tuboly, Andrea Szabó, Dénes Garab, Gábor Bartha, Ágnes Janovszky, Gábor Eros, Anna Szabó, A. Mohácsi, Gábor Szabó, J. Kaszaki, M. Ghyczy-, M. Borós

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Previous studies demonstrated methane generation in aerobic cells. Our aims were to investigate the methanogenic features of sodium azide (NaN3)-induced chemical hypoxia in the whole animal and to study the effects of L-α-glycerylphosphorylcholine (GPC) on endogenous methane production and inflammatory events as indicators of a NaN3-elicited mitochondrial dysfunction. Group 1 of Sprague-Dawley rats served as the sham-operated control; in group 2, the animals were treated with NaN3 (14 mg·kg-1·day-1 sc) for 8 days. In group 3, the chronic NaN3 administration was supplemented with daily oral GPC treatment. Group 4 served as an oral antibiotic-treated control (rifaximin, 10 mg·kg-1·day-1) targeting the intestinal bacterial flora, while group 5 received this antibiotic in parallel with NaN3 treatment. The whole body methane production of the rats was measured by means of a newly developed method based on photoacoustic spectroscopy, the microcirculation of the liver was observed by intravital videomicroscopy, and structural changes were assessed via in vivo fluorescent confocal laser-scanning microscopy. NaN3 administration induced a significant inflammatory reaction and methane generation independently of the methanogenic flora. After 8 days, the hepatic microcirculation was disturbed and the ATP content was decreased, without major structural damage. Methane generation, the hepatic microcirculatory changes, and the increased tissue myeloperoxidase and xanthine oxidoreductase activities were reduced by GPC treatment. In conclusion, the results suggest that methane production in mammals is connected with hypoxic events associated with a mitochondrial dysfunction. GPC is protective against the inflammatory consequences of a hypoxic reaction that might involve cellular or mitochondrial methane generation.

Original languageEnglish
JournalAmerican Journal of Physiology - Cell Physiology
Volume304
Issue number2
DOIs
Publication statusPublished - Jan 15 2013

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Sodium Azide
Methane
Glycerylphosphorylcholine
Microcirculation
rifaximin
Liver
Xanthine Dehydrogenase
Anti-Bacterial Agents
Video Microscopy
Hypoxia
Confocal Microscopy
Peroxidase
Sprague Dawley Rats
Mammals
Spectrum Analysis
Adenosine Triphosphate

Keywords

  • Hypoxia
  • Inflammation
  • L-α-glycerylphosphorylcholine
  • Methanogenesis

ASJC Scopus subject areas

  • Cell Biology
  • Physiology

Cite this

Methane biogenesis during sodium azide-induced chemical hypoxia in rats. / Tuboly, Eszter; Szabó, Andrea; Garab, Dénes; Bartha, Gábor; Janovszky, Ágnes; Eros, Gábor; Szabó, Anna; Mohácsi, A.; Szabó, Gábor; Kaszaki, J.; Ghyczy-, M.; Borós, M.

In: American Journal of Physiology - Cell Physiology, Vol. 304, No. 2, 15.01.2013.

Research output: Contribution to journalArticle

Tuboly, Eszter ; Szabó, Andrea ; Garab, Dénes ; Bartha, Gábor ; Janovszky, Ágnes ; Eros, Gábor ; Szabó, Anna ; Mohácsi, A. ; Szabó, Gábor ; Kaszaki, J. ; Ghyczy-, M. ; Borós, M. / Methane biogenesis during sodium azide-induced chemical hypoxia in rats. In: American Journal of Physiology - Cell Physiology. 2013 ; Vol. 304, No. 2.
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AU - Eros, Gábor

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AU - Mohácsi, A.

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AB - Previous studies demonstrated methane generation in aerobic cells. Our aims were to investigate the methanogenic features of sodium azide (NaN3)-induced chemical hypoxia in the whole animal and to study the effects of L-α-glycerylphosphorylcholine (GPC) on endogenous methane production and inflammatory events as indicators of a NaN3-elicited mitochondrial dysfunction. Group 1 of Sprague-Dawley rats served as the sham-operated control; in group 2, the animals were treated with NaN3 (14 mg·kg-1·day-1 sc) for 8 days. In group 3, the chronic NaN3 administration was supplemented with daily oral GPC treatment. Group 4 served as an oral antibiotic-treated control (rifaximin, 10 mg·kg-1·day-1) targeting the intestinal bacterial flora, while group 5 received this antibiotic in parallel with NaN3 treatment. The whole body methane production of the rats was measured by means of a newly developed method based on photoacoustic spectroscopy, the microcirculation of the liver was observed by intravital videomicroscopy, and structural changes were assessed via in vivo fluorescent confocal laser-scanning microscopy. NaN3 administration induced a significant inflammatory reaction and methane generation independently of the methanogenic flora. After 8 days, the hepatic microcirculation was disturbed and the ATP content was decreased, without major structural damage. Methane generation, the hepatic microcirculatory changes, and the increased tissue myeloperoxidase and xanthine oxidoreductase activities were reduced by GPC treatment. In conclusion, the results suggest that methane production in mammals is connected with hypoxic events associated with a mitochondrial dysfunction. GPC is protective against the inflammatory consequences of a hypoxic reaction that might involve cellular or mitochondrial methane generation.

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