Bisphenol A-induced toxicity in Drosophila melanogaster: Mitigation by vanillic acid and modulation of CncC/Keap1 pathway gene expression.

Bisphenol A (BPA) is a pervasive endocrine-disrupting chemical with documented toxic effects in living organisms. This study evaluated the protective potential of vanillic acid (VA) against BPA-induced toxicity in Drosophila melanogaster. BPA exposure elevated lipid peroxidation (MDA), reduced antioxidant defenses (SOD and CAT activities and GSH content), increased DNA damage (Comet assay), lowered acetylcholinesterase levels, and impaired developmental parameters (pupation, climbing, crawling, lifespan, and food intake). BPA also upregulated SOD, CAT, gclc, hsp70, CncC, and Keap1 mRNA expression, indicating activation of the cellular stress response. VA co-treatment dose-dependently mitigated these effects, restoring redox balance, reducing DNA strand breaks at the highest VA dose, and rescuing developmental endpoints. These findings suggest that VA is an effective natural protective agent against BPA toxicity in vivo, an effect accompanied by modulation of CncC/Keap1 pathway gene expression.