Model for the cometabolic biodegradation of chlorinated organics. Academic Article uri icon

abstract

  • A mechanistic model is developed to describe the kinetics of the cometabolic degradation of chlorinated organics by oxygenase-expressing cultures. The oxidization of chlorinated organics has been shown to cause decreased cell activity due to product toxicity and/or the depletion of reducing energy. In addition, competition between growth substrate and cometabolic substrate for oxygenase enzymes may significantly affect cometabolic degradation rates. Typical saturation kinetic expressions for substrate degradation (Michaelis-Menten equation) and cell growth (Monod equation) cannot adequately describe the behavior of these interacting effects. In this study, a modification of Michaelis-Menten/Monod kinetics is proposed that incorporates the effects of product toxicity, reducing energy limitation, and competitive inhibition together with cell growth and decay. This model is able to predict the kinetics of chlorinated organic degradation by oxygenase-expressing cultures over a range of substrate conditions (resting cells, cells with reducing energy substrate, cells with growth substrate). The effects of endogenous and external reducing energy sources on observed cometabolic degradation rates and transformation capacities (Kcob and Tcob) are discussed and verified by experimental results. © 1995, American Chemical Society. All rights reserved.

author list (cited authors)

  • Chang, H., & Alvarez-Cohen, L.

citation count

  • 105

publication date

  • September 1995