Mesotrione herbicide does not cause genotoxicity, but modulates the genotoxic effects of Atrazine when assessed in mixture using a plant test system (Allium cepa).

Mesotrione (MES) is an herbicide from the triketone family and has been used as an alternative to Atrazine (ATZ), which was banned in some countries due to its toxicity to non-target organisms. Despite being considered an eco-friendly herbicide, data from the literature about the harmful effects of MES in its pure form and/or in combination with other herbicides is still scarce. Aimed at assessing the potential of MES to induce cell death and DNA damage, seeds of Allium cepa (higher plant, monocotyledon) were exposed to this herbicide, pure and in mixture with ATZ, and the number of dividing cells (cytotoxicity), chromosomal aberrations (CA, genotoxicity) and micronuclei (MN, mutagenicity) were then quantified. The pure MES (1.8 to 460 µg/L) did not show either cytotoxicity or genotoxicity/mutagenicity under the tested conditions. The genotoxicity of ATZ (1.5 to 400 µg/L), previous reported in the literature, was confirmed herein. The assessment of MES + ATZ mixtures (1.8 + 1.5; 7 + 6.25; 30 + 25 µg/L, respectively) showed that MES, at low concentrations, enhance the genotoxicity of ATZ (potentiation), since the significant frequencies of CA and MN were greater than the ones expected in additive effects. Taking together, MES in its pure form seems to be a safe alternative to ATZ regarding the capacity to damage (at cellular and DNA levels) non-target plants (Monocots); however, MES in combination with ATZ appeared to act as a co-mutagen at low concentrations.

A multibiomarker evaluation of urban, industrial, and agricultural exposure of small characins in a large freshwater basin in southern Brazil.

Iguaçu River is the second most polluted river of Brazil. It receives agrochemicals and contaminants of urban and industrial sources along its course. A multibiomarker approach was employed here to evaluate the health of a small characin (Astyanax spp.) at two sites along the river, sampled during a dry (autumn) and a rainy (spring) season. Biomarkers were condition factor and somatic indices (gonads and liver); genetic damage (comet assay and micronucleus test); enzyme activities such as hepatic catalase (CAT) and glutathione S-transferase (GST), lipoperoxidation (LPO), branchial and renal carbonic anhydrase (CA), acetylcholinesterase (AChE) in the muscle and the brain, histopathology of the liver and gills, and concentrations of polycyclic aromatic hydrocarbons (PAHs) in bile. There were no consistent differences in biomarker responses between the two study sites. Some biomarkers revealed greater potential impact in the rainy season, when increased amounts of contaminants are washed into the river (combined CAT inhibition and LPO increase, CA upregulation). Other biomarkers, however, revealed potential greater impact in the dry season, when contaminants potentially concentrate (GST induction, AChE inhibition, and liver histopathological alterations). Although of a complex nature, field experiments such as this provide rich data for monitoring protocols and assessment of general risk of exposure to pollutants of river systems.