RESUMO
Atrazine is an herbicide commonly used in several countries. Due to its long half-life, associated with its use in large scales, atrazine residues remain as environmental pollutants in water bodies. Phytoremediation is often pointed out as an interesting approach to remove atrazine from the aquatic environment, but its practical application is limited by the high toxicity of this herbicide. Here, we characterize the damages triggered by atrazine in Pistia stratiotes, evaluating the role of nitric oxide (NO), a cell-signaling molecule, in increasing the tolerance to the pollutant and the phytoremediation potential of this species. Pistia stratiotes plants were exposed to four treatments: Control; Sodium nitroprusside (SNP) (0.05 mg L-1); Atrazine (ATZ) (150 µg L-1) and ATZ + SNP. The plants remained under those conditions for 24 h for biochemical and physiological analysis and 3 days for the evaluation of relative growth rate. The presence of atrazine in plant cells triggered a series of biochemical and physiological damages, such as the increase in the generation of reactive oxygen species, damages to cell membranes, photosynthesis impairment, and negative carbon balance. Despite this, the plants maintained greater growth rates than other aquatic macrophytes exposed to atrazine and showed high bioconcentration and translocation factors. The addition of SNP, a NO donor, decreased the herbicide toxicity, with an increase of over 60% in the IC50 value (Inhibitor Concentration). Indeed, the NO signaling action was able to increase the tolerance of plants to atrazine, which resulted in increments in pollutant uptake and translocation, with the maintenance of overall cell (e.g. membranes) and organs (root system) structure, and the functioning of central physiological processes (e.g. photosynthesis). These factors allowed for more quickly and efficient removal of the pollutant from the environment, reducing costs, and increasing the viability of the phytoremediation process.
