Scientific Reports (Aug 2017)

Excessive alcohol consumption induces methane production in humans and rats

  • E. Tuboly,
  • R. Molnár,
  • T. Tőkés,
  • R. N. Turányi,
  • P. Hartmann,
  • A. T. Mészáros,
  • G. Strifler,
  • I. Földesi,
  • A. Siska,
  • A. Szabó,
  • Á. Mohácsi,
  • G. Szabó,
  • M. Boros

DOI
https://doi.org/10.1038/s41598-017-07637-3
Journal volume & issue
Vol. 7, no. 1
pp. 1 – 10

Abstract

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Abstract Various studies have established the possibility of non-bacterial methane (CH4) generation in oxido-reductive stress conditions in plants and animals. Increased ethanol input is leading to oxido-reductive imbalance in eukaryotes, thus our aim was to provide evidence for the possibility of ethanol-induced methanogenesis in non-CH4 producer humans, and to corroborate the in vivo relevance of this pathway in rodents. Healthy volunteers consumed 1.15 g/kg/day alcohol for 4 days and the amount of exhaled CH4 was recorded by high sensitivity photoacoustic spectroscopy. Additionally, Sprague-Dawley rats were allocated into control, 1.15 g/kg/day and 2.7 g/kg/day ethanol-consuming groups to detect the whole-body CH4 emissions and mitochondrial functions in liver and hippocampus samples with high-resolution respirometry. Mitochondria-targeted L-alpha-glycerylphosphorylcholine (GPC) can increase tolerance to liver injury, thus the effects of GPC supplementations were tested in further ethanol-fed groups. Alcohol consumption was accompanied by significant CH4 emissions in both human and rat series of experiments. 2.7 g/kg/day ethanol feeding reduced the oxidative phosphorylation capacity of rat liver mitochondria, while GPC significantly decreased the alcohol-induced CH4 formation and hepatic mitochondrial dysfunction as well. These data demonstrate a potential for ethanol to influence human methanogenesis, and suggest a biomarker role for exhaled CH4 in association with mitochondrial dysfunction.