Multifaceted investigation of esfenvalerate-induced toxicity on Allium cepa L.

The objective of this study was to assess the toxicity of the insecticide esfenvalerate in Allium cepa, employing a multifaceted methodology. For this purpose, A. cepa bulbs were organized into four groups, one of which served as the control. The control group was exposed to tap water, while the remaining three groups were exposed to esfenvalerate at concentrations of 0.33 mg/L, 0.64 mg/L and 0.98 mg/L, respectively. The application of the highest dose of 0.98 mg/L esfenvalerate resulted in a significant decrease in physiological parameters, including a 51% reduction in rooting percentage, an 85.3% decrease in root elongation, and a 54.3% decrease in weight gain (p < 0.05). In the esfenvalerate-treated group (0.98 mg/L), a 45.7% decrease in mitotic index was observed, while a significant increase in chromosomal aberrations and micronucleus formation was observed compared to the control group (p < 0.05). The most frequently observed chromosomal abnormalities due to esfenvalerate were sticky chromosome, vagrant chromosome, fragment, unequal distribution of chromatin, bridge, vacuolated nucleus, reverse polarization and multipolar anaphase. Insecticide application could significantly increase the percentage of DNA tails up to 48.3%, as determined by the Comet test (p < 0.05). Exposure to 0.98 mg/L esfenvalerate increased malondialdehyde level (2.75-fold), proline level (1.96-fold), superoxide dismutase activity (1.35-fold), and catalase activity (1.69-fold) while reducing chlorophyll a level (58.18%) and chlorophyll b level (70.35%) (p < 0.05). Molecular docking analysis revealed that esfenvalerate can interact with tubulins, DNA topoisomerases, glutamate-1-semialdehyde aminotransferase, protochlorophyllide reductase and DNA molecules. Epidermis and cortex cell damages, cortex cell wall thickening, material accumulation in cortex cells and flattened cell nucleus were recorded as meristematic cell damages due to esfenvalerate. The toxicological profile of esfenvalerate on A. cepa exhibited dose dependence. While esfenvalerate-induced oxidative stress is the most probable cause of toxicity, direct interaction with DNA and other molecules that play a crucial role in maintaining cell integrity may also be among the mechanisms of toxicity. The study's findings emphasize that esfenvalerate poses a risk to non-target organisms, underscoring the need for a reassessment of its regulations and further research into its toxicity.