An integral concept of the primary and secondary targets for chlorophenolic toxicants in luminescent bacteria has not been developed, in spite of the fact that photobacteria are used on a large scale as biosensors for these and other toxic compounds [1][2][3]. As a rule, the main attention is paid to comparative analysis of toxicities of certain classes of chemical compounds versus structural parameters of their molecules [2,3]. The mechanism of action of chlorophenols on bacterial structures is an important topic not only for biodetection but also for an understanding of the processes involved in microbiological degradation of these substances [4,5]. Both the interaction of a toxicant with bacterial luciferase and the mediated response of the bioluminescent system to other processes (first and foremost, those controlling the formation of luciferase substrates-reduced flavin and long-chain aliphatic aldehyde) may determine the effect of xenobiotics on the luminescence of bacterial cells [6].Many papers [7-9] consider the plasma membrane as the primary target of chloroaromatic toxicants. Absorption of toxicants changes the physical characteristics of the membrane, which disrupts membrane functions and, correspondingly, influences cell viability and growth [9]. The fact that the efficiency of chlorophenolic toxicants increases with the hydrophobicity of their molecule is interpreted as a proof of the membrane action of these compounds. As was demonstrated in experiments with Escherichia coli cells carrying cloned luciferase genes [10], the toxic effect increased with the number of chlorine atoms in the chlorophenol molecule. The same pattern was observed in analyzing the effect of chlorinated phenols and phenoxyacetic acids on Vibrio harveyi cells [6]. Note that the enzymatic complexes of the bioluminescent system are associated with the bacterial plasma membrane [11]. The damage of the membrane structural and functional organization by chlorophenols should in any case influence the cell luminescent reaction.The organochlorinated compounds chosen for this work, namely, 2,4-di-and 2,4,5-triphenoxyacetic acids (2,4-D and 2,4,5-T), belong to the so-called bifunctional inhibitors [12] with the properties of weak acids (pK ~ 2.6 ), possessing a hydrophobic aromatic core and a carboxyl group. As a rule, such compounds interact with biological structures via the aromatic core, followed by the reaction of the acid group with the corresponding binding centers. The hydrophobicity of the toxin molecule is the determining parameter. The efficiency of such compounds depends on the pH of the medium; moreover, the pH influences the energy and metabolic potential of the cell, on the one hand, thereby affecting emission kinetics and intensity, and the dissociation of the toxicant and the membrane surface charge, on the other hand. The combination of these processes may influence the binding of the toxicant and its transfer into the cell.Only sparse data about the effect of pH on the toxicity of chlorophenols may be found in the lit...