Difference between revisions of "Tuboly 2017 Sci Rep"
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|area=Respiration, Exercise physiology;nutrition;life style | |area=Respiration, Exercise physiology;nutrition;life style | ||
|injuries=Oxidative stress;RONS | |||
|organism=Rat | |organism=Rat | ||
|tissues=Nervous system, Liver | |tissues=Nervous system, Liver | ||
|preparations=Homogenate | |preparations=Homogenate | ||
|couplingstates= | |couplingstates=OXPHOS | ||
|pathways= | |pathways=Gp | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=Labels, 2018-03 | |additional=Labels, 2018-03 | ||
}} | }} |
Revision as of 10:17, 6 March 2018
Tuboly E, MolnĂĄr R, TĆkĂ©s T, TurĂĄnyi RN, Hartmann P, MĂ©szĂĄros AT, Strifler G, Földesi I, Siska A, SzabĂł A, MohĂĄcsi Ă, SzabĂł G, Boros M (2017) Excessive alcohol consumption induces methane production in humans and rats. Sci Rep 7:7329. |
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 1.15âg/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, 1.15âg/kg/day and 2.7âg/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. 2.7âg/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.
âą Bioblast editor: Kandolf G, Meszaros AT âą 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: Gp
HRR: Oxygraph-2k
Labels, 2018-03