Abstract

Research on herbicide biosensors based on plant photosystem II (PS II) or on reaction centers of purple bacteria (BRC) has been on-going for the past decade. Herbicides inhibit functioning of the PS II by competitively binding to the QB plastoquinone binding site. The structural similarity between nitric explosives and nitrophenolic- and atrazine-type herbicides inspired us to explore whether nitric explosives would inhibit photosynthesis via the same mechanism (involving Q B site) as the herbicides. The design of the explosives biosensor was similar to that of the biosensors for herbicides. The detection was achieved by photo-electrochemical methods, employing PS II immobilized on a screen-printed electrode as a part of electrical circuit; optical spectroscopy was used as a supplementary method. We have demonstrated that this electrochemical biosensor is capable of detecting explosives such as picric acid, TNT and tetryl. The magnitude of the peak current induced by illumination depends on the concentration of the explosive in the same manner as in the case of herbicides, which suggests that Q B binding site is indeed involved in the PS II inhibition of the selected explosive compounds. However, the limits of detection for explosives, especially for TNT, appear to be higher (i.e. worse) than for the herbicides. Modeling of photosynthesis inhibitor docking on PS II has also been performed to determine the reasons for poor TNT detection