Homoacetogenesis and microbial community composition are shaped by pH and total sulfide concentration

Eleftheria Ntagia, Ioanna Chatzigiannidou, Adam J. Williamson, Jan B. A. Arends, Korneel Rabaey

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Biological CO2 sequestration through acetogenesis with H2 as electron donor is a promising technology to reduce greenhouse gas emissions. Today, a major issue is the presence of impurities such as hydrogen sulfide (H2S) in CO2 containing gases, as they are known to inhibit acetogenesis in CO2-based fermentations. However, exact values of toxicity and inhibition are not well-defined. To tackle this uncertainty, a series of toxicity experiments were conducted, with a mixed homoacetogenic culture, total dissolved sulfide concentrations ([TDS]) varied between 0 and 5 mM and pH between 5 and 7. The extent of inhibition was evaluated based on acetate production rates and microbial growth. Maximum acetate production rates of 0.12, 0.09 and 0.04 mM h-1 were achieved in the controls without sulfide at pH 7, pH 6 and pH 5. The half-maximal inhibitory concentration (IC50qAc) was 0.86, 1.16 and 1.36 mM [TDS] for pH 7, pH 6 and pH 5. At [TDS] above 3.33 mM, acetate production and microbial growth were completely inhibited at all pHs. 16S rRNA gene amplicon sequencing revealed major community composition transitions that could be attributed to both pH and [TDS]. Based on the observed toxicity levels, treatment approaches for incoming industrial CO2 streams can be determined.
Original languageEnglish (US)
JournalMicrobial Biotechnology
StatePublished - Mar 3 2020
Externally publishedYes

Bibliographical note

KAUST Repository Item: Exported on 2020-10-01
Acknowledgements: KR is supported by the European Regional Development Fund through the Interreg V program Flanders-the Netherlands (project #0165 ‘EnOp’). KR is also supported by KAUST (Project # OSR-2016-CRG5-2985). EN and IC are supported by UGent. All authors acknowledge the support of BOF Basisinfrastructuur (Grant No. 01B05912) for equipment used in this study. The authors thank Tim Lacoere (CMET, UGent) for performing the 16S rRNA gene amplicon sequencing and the cloning library data analysis. The authors thank Jo Philips and Erika Fiset (CMET, UGent) for critically commenting on the manuscript and Greet Van de Velde (CMET, UGent) for assisting with the IC analyses.
This publication acknowledges KAUST support, but has no KAUST affiliated authors.


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