A cometabolic kinetics model incoroporating enzyme inhibition, inactivation, and recovery: II. Trichloroethylene degradaation experiments.

A Cometabolism enzyme kinetics model has been presented which takes into account changes in bacterial activity associated with enzyme inhibitiion, inactivation, inactivation of enzyme resulting from product toxicty, 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-staate under certain conditions. In its simplified from, the model also assumes that enzyme inactivation is directly propoertional to nongrawth substrate oxidation, and that recovery is directly proportionla to growth substrate oxidation. In part 1, model drivation, simplification, and analyses were described. In this articles, model assuptiions are tested by analyzing data from experiments exmining trichloroethylene (TCE) degradation by the ammoniaoxidizing baceterium Nitrosomonas europaea in a quasisteady-state bioreactor. Model solution results showed steady-state bioreactor. Model solution results showed TCE to be a competitive inhibitoer 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 fo 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(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 adn 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 understandign the effects fo TCE on AMO function and bacterial response. The model assumptions were verified except tht questions remain regarding the factores controlling recovery and its role in the long term. (c) 1995 John Wiley & Sons, Inc.