Open AccessExcessive alcohol consumption induces methane production in humans and rats
Author(s) -
Eszter Tuboly,
Regina Molnár,
Tímea Tőkés,
R. N. Turányi,
Petra Hartmann,
András Mészáros,
Gerda Strifler,
Imre Földesi,
Andrea Siska,
Anna Szabó,
Árpád Mohácsi,
Gábor Szabó,
Mihály Boros
Publication year - 2017
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/s41598-017-07637-3
Subject(s) - ethanol , alcohol , mitochondrion , methanogenesis , oxidative stress , oxidative phosphorylation , liver injury , chemistry , biochemistry , in vivo , ethanol metabolism , medicine , biology , endocrinology , methane , microbiology and biotechnology , organic chemistry
Various studies have established the possibility of non-bacterial methane (CH 4 ) 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-CH 4 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 CH 4 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 CH 4 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 CH 4 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 CH 4 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 CH 4 in association with mitochondrial dysfunction.