Mechanisms and Models for Inhibition and Toxicity

The mechanisms by which XOCs inhibit microbial growth and substrate removal are not well-defined and have only recently become of interest. Consequently, our knowledge of the subject is rather limited. Nevertheless, one would think that the mechanisms are probably the same for inhibition and toxicity, with reaction rates becoming progressively slower as more damage occurs until ultimately the cumulative damage is sufficient to disrupt all activity and we say that toxicity has occurred.

Some XOCs have very specific effects on microbial cells, whereas others have a more general or nonspecific effect. Among the specific effects are radical forming reactions by transition metals, forming hydroxyl radicals that react with a broad range of macromolecules; reactions of organic acids with thiol groups in enzymes, changing their conformation, and thus their reaction rates; formation of covalent bonds with amino acid side-chains in enzymes, altering the conformation of the active site; and interference with protein synthesis. In addition, XOCs that are analogs of biogenic organic compounds can bind irreversibly with the active site on an enzyme, blocking its activity.

A good example of a nonspecific effect is provided by the action of hydrocarbons.49 Many hydrocarbons are amphiphilic, i.e., they contain both hydrophobic and hydrophilic moieties. As such they behave like the phospholipids that form cellular membranes, making them soluble in those membranes. As hydrocarbons dissolve in the membrane, they disrupt its structural integrity, thereby interfering with its major functions, which are to serve as a barrier separating the cytoplasm from the environment, provide for energy transduction, and provide spatial organization for certain enzymes. At low concentrations, alteration of these functions merely reduces the activity of the cell. However, as the concentration of the hydrocarbon in the environment is increased its concentration in the membrane also increases, thereby causing greater disruption and a greater effect. Ultimately, when the concentration is sufficiently high, the cell stops functioning.

Models for inhibition quantify the effects by altering the values of |1 and Ks associated with carbon oxidation or nitrification. Although several have been proposed, the most general is that of Han and Levenspiel,27 which was given as Eq.

Table 22.1 Types of Inhibition







on p.

of n

on Ks

of m



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