Loading…
Acetogenesis from H2 and CO2 by methane- and non-methane-producing human colonic bacterial communities
Abstract The purpose of the study was to define the potential for reductive acetogenesis of colonic microflora from six non\u2010methane\u2010 and four methane\u2010excreting human subjects in relation to numbers of the different H2\u2010utilizing microorganisms. Faecal bacterial suspensions were in...
Saved in:
Published in: | FEMS microbiology ecology 1996-03, Vol.19 (3), p.193-202 |
---|---|
Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Abstract
The purpose of the study was to define the potential for reductive acetogenesis of colonic microflora from six non\u2010methane\u2010 and four methane\u2010excreting human subjects in relation to numbers of the different H2\u2010utilizing microorganisms. Faecal bacterial suspensions were incubated in the presence of NaH13CO3 and under a gas phase composed of either 100% N2 (control) or 80% H2\u201320% N2. The effects of a specific methanogenesis inhibitor or of sulfate supplementation were also determined. Quantitative nuclear magnetic resonance showed the presence of both single\u2010 and double\u2010labelled acetate in all incubations under hydrogen. H2/CO2\u2010acetogenesis appears to be a quantitatively important activity only in the presence of very low numbers of methanogens. Inhibition of methanogenesis induced a large increase in 13CO2 incorporation into acetate in CH4\u2010producing samples. These results showed that methanogens can efficiently outcompete acetogens in human colonic contents. In contrast, no clear\u2010cut competition for H2 between acetogenesis and dissimilatory sulfate\u2010reduction could be demonstrated. A slight reduction of the acetogenic activity was only observed at the highest sulfate addition (100 mM). |
---|---|
ISSN: | 0168-6496 1574-6941 |
DOI: | 10.1111/j.1574-6941.1996.tb00212.x |