Tuboly 2017 Sci Rep: Difference between revisions

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Latest revision as of 11:17, 6 March 2018

Publications in the MiPMap
Tuboly E, MolnΓ‘r R, TΕ‘kΓ©s T, TurΓ‘nyi RN, Hartmann P, MΓ©szΓ‘ros AT, Strifler G, FΓΆldesi I, Siska A, SzabΓ³ A, MohΓ‘csi Á, SzabΓ³ G, Boros M (2017) Excessive alcohol consumption induces methane production in humans and rats. Sci Rep 7:7329.

Β» PMID: 28779149 Open Access

Tuboly E, Molnar R, Tokes T, Turanyi RN, Hartmann P, Meszaros AT, Strifler G, Foeldesi I, Siska A, Szabo A, Mohacsi A, Szabo G, Boros M (2017) Sci Rep

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.

β€’ Bioblast editor: Kandolf G, Meszaros AT β€’ O2k-Network Lab: HU Szeged Boros M


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Stress:Oxidative stress;RONS  Organism: Rat  Tissue;cell: Nervous system, Liver  Preparation: Homogenate 


Coupling state: OXPHOS  Pathway:HRR: Oxygraph-2k 

Labels, 2018-03 

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