Premium
Growth kinetics of Pseudomonas putida in cometabolism of phenol and 4‐chlorophenol in the presence of a conventional carbon source
Author(s) -
Wang SiJing,
Loh KaiChee
Publication year - 2000
Publication title -
biotechnology and bioengineering
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.136
H-Index - 189
eISSN - 1097-0290
pISSN - 0006-3592
DOI - 10.1002/(sici)1097-0290(20000520)68:4<437::aid-bit9>3.0.co;2-g
Subject(s) - pseudomonas putida , cometabolism , phenol , chemistry , substrate (aquarium) , kinetics , cell growth , non competitive inhibition , growth inhibition , biochemistry , chromatography , biology , organic chemistry , bacteria , enzyme , ecology , physics , quantum mechanics , bioremediation , genetics
Growth kinetics of Pseudomonas putida (ATCC 49451) in cometabolism of phenol and 4‐chlorophenol (4‐cp) in the presence of sodium glutamate (SG) were studied. In the ternary substrate mixture, phenol and SG are growth substrates while 4‐cp is a nongrowth substrate. Cell growth on phenol was found to follow Andrews kinetics and cells displayed substrate inhibition pattern on sodium glutamate in the range of 0–4 g L −1 as well. A cell growth model for the ternary substrate system was established based on a simplified cell growth mechanism and subsequently modified by experimental results. Model analysis over a wide range of substrate concentrations shows that the inhibition of SG is much larger than phenol at low phenol concentrations (⩽200 mg L −1 ) while phenol exerts dominant inhibition on cell growth at higher phenol concentrations (⩾600 mg L −1 ). The nongrowth substrate, 4‐cp, inhibits cell growth mainly through inactivation of cells (cell decay) and competitive inhibition to cell growth on phenol. In the absence of SG, 4‐cp retards cell growth severely and cells cannot grow at 250 mg L −1 4‐cp. Addition of sodium glutamate, however, greatly attenuates the toxicity of 4‐cp and supports cell growth at 4‐cp concentration higher than 250 mg L −1 . By using the proposed cell growth model, we were able to optimize the amount of SG needed to enhance cell growth rate and validate model predictions against experimental data. © 2000 John Wiley & Sons, Inc. Biotechnol Bioeng 68: 437–447, 2000.