Evaluation of the genotoxic activity of dicamba and atrazine herbicides in several Mexican and South American varieties of sweetcorn (Zea mays L.)

• Published in: Genetics and molecular research 2015-12, Vol.14 (4), p.16585-16593
• Main Authors: Reynoso, M S, Alvarez, C M, De la Cruz, L, Escoto, M D, Sánchez, J J G
• Format: Article
• Language: English
• Subjects: Atrazine - adverse effects; Atrazine - toxicity; Dicamba - adverse effects; Dicamba - toxicity; DNA Damage; Herbicides - adverse effects; Herbicides - toxicity; Zea mays; Zea mays - drug effects; Zea mays - genetics
• ISSN: 1676-5680; 1676-5680
• DOI: 10.4238/2015.December.11.5

Corn is a major crop and various herbicides are used to maximize its production, which include a dicamba-atrazine mixture. This has great advantages, but can also induce DNA damage. Genotoxic activity was assessed by comet assay following application of two concentrations of dicamba-atrazine: 1000-2000 and 2000-4000 ppm. Apical meristem leaf nuclei from 119 varieties of sweetcorn plants from Mexico and South America, and from five commercial sweetcorn hybrids were used. Each accession comprised two individuals per concentration and two controls. Significant genotoxic activity (P < 0.001) was observed following treatment with 1000-2000 and 2000-4000 ppm compared to the negative control. There was no difference in the genotoxic activity induced by both 1000-2000 and 2000-4000 ppm concentrations in plants from Mexico and South America (P > 0.05) except (P < 0.05) in the 2000-4000 ppm treated plants from Mexico and the 1000-2000 ppm treated plants from South America. Sweetcorn hybrids showed significant genetic damage (P < 0.01) at all concentrations compared to the negative controls. Thus, the dicamba-atrazine mixture caused genetic damage to corn plants, and it suggested that Mexican sweetcorn is more sensitive to dicamba-atrazine than the maize varieties from South America. Neither hybrid status nor the origin avoids DNA damage caused by Marvel. Thus, maize can be useful as a biomonitor of genetic damage induced by chemicals and to identify possible phenotypes based upon the amount of genetic damage induced by herbicides and selection of resistant genotypes.