Models for Reversible and Unreversible Inhibitions of Biological Nitrite Oxidation

  • LIU Bing
    Faculty of Environmental Engineering, The University of Kitakyushu
  • GOEL Rajeev
    Hydromantis Environmental Software Solutions Inc.
  • TERASHIMA Mitsuharu
    Faculty of Environmental Engineering, The University of Kitakyushu
  • YASUI Hidenari
    Faculty of Environmental Engineering, The University of Kitakyushu

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Other Title
  • 亜硝酸酸化細菌の反応を例とした可逆的および不可逆的阻害現象の理論的考察
  • アショウサン サンカ サイキン ノ ハンノウ オ レイ ト シタ カギャクテキ オヨビ フカギャクテキ ソガイ ゲンショウ ノ リロンテキ コウサツ

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Abstract

 Biological reactions often experience inhibition conditions from high concentration of substrate, reaction products or other external inhibitory compounds. The inhibitory compounds may affect the enzymatic system leading to different forms of competitive, non-competitive or uncompetitive reversible enzyme inhibition. In other situations, the concentration of inhibitory compound could result in enzyme poisoning leading to irreversible inhibition. There are several mathematical models to express reversible inhibition, however recovery/adaptation phenomenon is not well described by these models. Furthermore, the modelling approaches for unreversible inhibitions are not well developed. In this study, dynamic response of oxygen uptake rate from nitrite oxidising batch experiments were used to develop models for reversible and irreversible inhibitions. The OUR batch tests from nitrite oxidation experiments conducted for nitrite-N concentration range of 125-2,000 mg-N /L revealed that the inhibition effect of free nitrous acid (FNA) and free ammonia (FA) disappeared after several hours due to microbial adaptation from the shock loading. The OUR tests also indicated irreversible inhibition (poisoning) leading to permanent reduction in activity at higher doses of inhibitory compounds For the reversible inhibition a time-dependent switching function was defined to express the degree of the adaptation. The irreversible poisoning phenomenon was defined as an additional first-order type decay/death process that was initiated when the inhibitory concentration exceeded the threshold level. The modified model developed from the batch experiments data was able to reasonably reproduce the effluent nitrogenous concentration in the WERF benchmark dataset of over 250 days.

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