Excessive alcohol consumption induces methane production in humans and rats

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 e...

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Autores principales:	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
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e780a57fba2444beb443ed67459b6788
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spelling	oai:doaj.org-article:e780a57fba2444beb443ed67459b67882021-12-02T15:05:42ZExcessive alcohol consumption induces methane production in humans and rats10.1038/s41598-017-07637-32045-2322https://doaj.org/article/e780a57fba2444beb443ed67459b67882017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07637-3https://doaj.org/toc/2045-2322Abstract 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.E. TubolyR. MolnárT. TőkésR. N. TurányiP. HartmannA. T. MészárosG. StriflerI. FöldesiA. SiskaA. SzabóÁ. MohácsiG. SzabóM. BorosNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q 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 Excessive alcohol consumption induces methane production in humans and rats
description	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.
format	article
author	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
author_facet	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
author_sort	E. Tuboly
title	Excessive alcohol consumption induces methane production in humans and rats
title_short	Excessive alcohol consumption induces methane production in humans and rats
title_full	Excessive alcohol consumption induces methane production in humans and rats
title_fullStr	Excessive alcohol consumption induces methane production in humans and rats
title_full_unstemmed	Excessive alcohol consumption induces methane production in humans and rats
title_sort	excessive alcohol consumption induces methane production in humans and rats
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/e780a57fba2444beb443ed67459b6788
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Excessive alcohol consumption induces methane production in humans and rats

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