Toxic effects and oxidative stress in higher plants exposed to polycyclic aromatic hydrocarbons and their N-heterocyclic derivatives.

N-heterocyclic derivatives of polycyclic aromatic hydrocarbons (NPAHs) are widespread concomitantly with their parent analogues and have been detected in air, water, sediments, and soil. Although they were shown to be highly toxic to some organisms, our understanding of their occurrence, environmental fate, biological metabolism, and effects is limited. This study evaluated toxic effects of three homocyclic aromatic hydrocarbons (PAHs-phenanthrene, anthracene, fluorene) and their seven N-heterocyclic derivates on higher terrestrial plants Sinapis alba, Triticum aestivum, and Phaseolus vulgaris. Germinability, morphological endpoints, parameters of detoxification, and antioxidant components of plant metabolism as well as lipid peroxidation were studied in acute phytotoxicity tests. Phytotoxicity of NPAHs was generally more pronounced than the effects of parent PAHs, and it significantly differed with respect to the structure of individual NPAHs. Sinapis alba and T. aestivum were more sensitive plant species than P. vulgaris. Chemicals with the strongest inhibition effect on germination and growth of plants were phenanthridine, acridine, benzo[h]quinoline, and 1,10- and 1,7-phenanthroline. All tested chemicals significantly induced activities of detoxification and antioxidant enzymes (glutathione reductase, glutathione peroxidase, and glutathione-S-transferase) at nanomolar to low micromolar concentrations. Levels of reduced glutathione were induced by all tested chemicals except 1,10- and 4,7-phenanthroline. Furthermore, fluorene, carbazole, acridine, phenanthrene, phenanthridine, benzo[h]quinoline, and 1,7-phenanthroline significantly increased lipid peroxidation. The results of our study newly demonstrate significant toxicity of NPAHs to plants and demonstrate suitability of multiple biomarker assessment to characterize mechanisms of oxidative stress and to serve as an early warning of phytotoxicity in vivo.