Toxicidade de doses subletais do herbicida Imazapyr sobre o desenvolvimento pós-embrionário e balanço redox de Drosophila melanogaster

Abstract

Modern agriculture is primarily characterized by extensive use of pesticides, particularly herbicides and insecticides. Imidazolinone herbicides, such as imazapyr, are widely used due to their selectivity in inhibiting the enzyme acetolactate synthase, affecting amino acid synthesis in weeds. However, several studies have shown that non-specific toxicity mechanisms can make herbicides extremely toxic to non-target organisms, particularly at sublethal concentrations. The effects of the herbicide imazapyr on non-target organisms are poorly understood, necessitating research to assess its toxicity. The fruit fly, Drosophila melanogaster, stands out as an ideal model for evaluating the toxicity of herbicides like imazapyr due to its rapid life cycle and cost-effectiveness. Thus, the aim of this study was to evaluate sublethal concentrations of the herbicide imazapyr on post-embryonic development in Drosophila melanogaster. Sublethal concentrations were determined through the median lethal concentration (LC50). Subsequently, animals at different stages of development were exposed to sublethal concentrations, and various changes in post-embryonic development were quantified, along with alterations in the pattern of redox homeostasis. We observed developmental delays, increased larval mortality, and decreased pupation and eclosion rates. Using the hydrogen peroxide biosensor (roGFP-Orp1), we observed that exposure to imazapyr resulted in mitochondrial redox imbalance, evidenced by increased H₂O₂ levels in the fat body. Furthermore, there were alterations in the enzymatic activity of antioxidant biomarkers, indicating a state of redox balance. These results highlight the high toxicity of imazapyr on post-embryonic development in Drosophila melanogaster at sublethal concentrations.