A cometabolic kinetics model incorporating enzyme inhibition, inactivation, and recovery. II: Trichloroethylene degradation experiments

• Published in: Biotechnology and bioengineering 1995, Vol.46 (3), p.232-245
• Main Authors: ELY, R. L, HYMAN, M. R, ARP, D. J, GUENTHER, R. B, WILLIAMSON, K. J
• Format: Article
• Language: English
• Subjects: Ammonia; Biological and medical sciences; Biology of microorganisms of confirmed or potential industrial interest; Biotechnology; Fundamental and applied biological sciences. Psychology; Mission oriented research; Nitrosomonas europaea; Physiology and metabolism
• ISSN: 0006-3592; 1097-0290

A cometabolism enzyme kinetics model has been presented which takes into account changes in bacterial activity associated with enzyme inhibition, inactivation of enzyme resulting from product toxicity, and respondent synthesis of new enzyme. Although this process is inherently unsteady-state, the model assumes that cometabolic degradation of a compound exhibiting product toxicity can be modeled as pseudo-steady-state under certain conditions. In its simplified form, the model also assumes that enzyme inactivation is directly proportional to nongrowth substrate 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 tested by analyzing data from experiments examining trichloroethylene (TCE) degradation by the ammonia-oxidizing bacterium Nitrosomonas europaea in a quasi-steady-state bioreactor. Model solution results showed TCE to be a competitive inhibitor of ammonia oxidation, with TCE affinity for ammonia monooxygenase (AMO) being about four times greater than that of ammonia for the enzyme. Inhibition was independent of TCE oxidation and occurred essentially instantly upon exposure to TCE. In contrast, inactivation of AMO occurred more gradually and was proportional to the rate and amount of TCE oxidized. Evaluation of other O sub(2)-dependent enzymes and electron transport proteins suggested that TCE-related damage was predominantly confined to AMO. In response to inhibition and/or inactivation, bacterial recovery was initiated, even in the presence of TCE, implying that membranes and protein synthesis systems were functioning. Analysis of data and comparison of model results showed the inhibition/inactivation/recovery concept to provide a reasonable basis for understanding the effects of TCE on AMO function and bacterial response. The model assumptions were verified except that questions remain regarding the factors controlling recovery and its role in the long term.