
Water Science and Technology Vol 38 No 2 pp 5561 © IWA Publishing 1998
The effects of macromolecular substrates and a metabolic inhibitor on volatile fatty acid metabolism in thermophilic aerobic digestion
A. Chu* and D. S. Mavinic**
*Department of Civil Engineering, University of Calgary, 2500 University Drive N.W. Calgary, Alberta, T2N 1N4 Canada
**Environmental Engineering Group, Department of Civil Engineering, University of British Columbia, 2324 Main Mall Vancouver, B.C., V6T 1W5 Canada
ABSTRACT
The effects of spiking macromolecular substrates and an inhibitor on the metabolic behavioral patterns of thermophilic aerobic digestion (TAD) biomass, from a pilot scale system, were studied. The 3 macromolecules examined were linoleic acid (lipid), peptone (protein) and dextrin (carbohydrates). Linoleic acid did very little in terms of volatile fatty acid (VFA) stimulation in either anaerobic or microaerobic environments. Dextrin stimulated propionate and acetate production in a rough 2 propionate to 1 acetate molar ratio under anaerobic conditions. Peptone was the only one of the three tested substrates that stimulated only acetate production under fermentative conditions. Under microaerobic conditions (oxygen demand exceeds oxygen supply), both peptone and dextrin stimulated the production of acetate. The results seen under both anaerobic and microaerobic experimental conditions, with the exception of linoleic acid, in so far as redox balance is concerned, are consistent with the hypothesized biochemical mechanisms describing substrate metabolism in TAD proposed by Chu et al. (1996). Since fermentative reactions do not utilize oxidative phosphorylation to produce energy, 2,4-dinitrophenol had no measurable effect on VFA metabolism in an anaerobic environment. The effect of this agent under microaerobic conditions, was to induce the process biomass to switch from generating energy via oxidative means to using substrate level phosphorylation reactions. This results in the accumulation of large amounts of acetate in excess of the control condition that was not treated with 2,4-dinitrophenol, since acetate production from acetyl-Coenzyme A yields energy.
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