NEUROPROTECTIVE AND ANTIOXIDANT EFFECTS OF Senecio brasiliensis EXTRACT AGAINST CHLORPYRIFOS TOXICITY IN Drosophila melanogaster

Resumo

INTRODUCTION: Chlorpyrifos is an organophosphate insecticide that induces neurotoxicity through irreversible inhibition of acetylcholinesterase (AChE), in addition to disrupting redox homeostasis. These mechanisms raise significant concerns in occupational exposures, being associated with human occupational exposure as well as non-target organisms like fishes and pollinator insects which are linked to adverse human health effects.  Recent studies highlight the pharmacological potential of plant-derived bioactive compounds, with Senecio brasiliensis (Pampa biome native) emerging as a significant source of these therapeutic molecules. OBJECTIVE: This study aimed to evaluate the protective potential of a hydroalcoholic extract of S. brasiliensis against chlorpyrifos-induced toxicity in Drosophila melanogaster. MATERIAL AND METHODS: Female Harwich strain flies (3-5 days old) were distributed into four experimental groups: control (1% sucrose), S. brasiliensis (1 mg/mL), chlorpyrifos (0.25 ppm), and combined treatment (insecticide + extract), with exposure for 48 hours. To assess the protective potential of the extract, AChE activity and non-protein thiol (NPSH) levels were quantified using Ellman’s method, reactive oxygen species (ROS) production was measured via DCFH-DA oxidation, lipid peroxidation was evaluated by thiobarbituric acid reactive substances (TBARS), nitric oxide (NO) levels were determined using the Griess method, cell viability was assessed via resazurin assay, and enzymatic activities of catalase (CAT), glutathione-S-transferase (GST), and superoxide dismutase (SOD) were analyzed. RESULTS AND CONCLUSION: Chlorpyrifos exposure inhibited AChE activity, a classic marker of organophosphate poisoning, and induced oxidative stress in D. melanogaster, characterized by increased ROS, lipid peroxidation, decreased NPSH, and suppressed CAT and GST activity. SOD activity remained unchanged, possibly due to adaptation of the antioxidant system. The redox imbalance was associated with impaired cell viability and activation of inflammatory pathways, evidenced by increased NO, a pro-inflammatory molecule. Treatment with S. brasiliensis extract showed a protective effect, reversing AChE inhibition and restoring redox homeostasis in the evaluated parameters, demonstrating its neuroprotective and antioxidant action. However, there was no improvement in cell viability, possibly due to irreversible cellular damage previously induced by chlorpyrifos. These results suggest that the bioactive compounds present in S. brasiliensis extract may mitigate acute damage caused by organophosphates, although early interventions are essential to preserve cell viability.