A COMETABOLIC KINETICS MODEL INCORPORATING ENZYME-INHIBITION, INACTIVATION, AND RECOVERY .2. TRICHLOROETHYLENE DEGRADATION EXPERIMENTS

Citation
Rl. Ely et al., A COMETABOLIC KINETICS MODEL INCORPORATING ENZYME-INHIBITION, INACTIVATION, AND RECOVERY .2. TRICHLOROETHYLENE DEGRADATION EXPERIMENTS, Biotechnology and bioengineering, 46(3), 1995, pp. 232-245
Citations number
27
Categorie Soggetti
Biothechnology & Applied Migrobiology
ISSN journal
00063592
Volume
46
Issue
3
Year of publication
1995
Pages
232 - 245
Database
ISI
SICI code
0006-3592(1995)46:3<232:ACKMIE>2.0.ZU;2-M
Abstract
A cometabolism enzyme kinetics model has been presented which takes in to account changes in bacterial activity associated with enzyme inhibi tion, inactivation of enzyme resulting from product toxicity, and resp ondent synthesis of new enzyme. Although this process is inherently un steady-state, the model assumes that cometabolic degradation of a comp ound exhibiting product toxicity can be modeled as pseudo-steady-state under certain conditions. In its simplified form, the model also assu mes that enzyme inactivation is directly proportional to nongrowth sub strate oxidation, and that recovery is directly proportional to growth substrate oxidation. In part 1, model derivation, simplification, and analyses were described. In this article, model assumptions are teste d by analyzing data from experiments examining trichloroethylene (TCE) degradation by the ammonia-oxidizing bacterium Nitrosomonas europaea in a quasisteady-state bioreactor. Model solution results showed TCE t o be a competitive inhibitor of ammonia oxidation, with TCE affinity f or ammonia monooxygenase (AMO) being about four times greater than tha t of ammonia for the enzyme. inhibition was independent of TCE oxidati on and occurred essentially instantly upon exposure to TCE. In contras t, inactivation of AMO occurred more gradually and was proportional to the rate and amount of TCE oxidized. Evaluation of other O-2-dependen t enzymes and electron transport proteins suggested that TCE-related d amage was predominantly confined to AMO. In response to inhibition and /or inactivation, bacterial recovery was initiated, even in the presen ce of TCE, implying that membranes and protein synthesis systems were functioning. Analysis of data and comparison of model results showed t he inhibition/inactivation/recovery concept to provide a reasonable ba sis for understanding the effects of TCE on AMO function and bacterial response. The model assumptions were verified except that questions r emain regarding the factors controlling recovery and its role in the l ong term. (C) 1995 John Wiley & Sons, Inc.