<i>Tapinanthus globiferus</i> mitigates arsenic-induced oxidative stress and genetic dysregulation In vivo

Environmental toxins such as sodium arsenite induce oxidative stress, disrupt redox homeostasis, and trigger oncogenic signaling, providing a model for studying natural redox modulators. This study investigated the protective effects of <i>Tapinanthus globiferus</i> fractions (butanol, methanol, and ethyl acetate) on sodium arsenite-exposed <i>Drosophila melanogaster.</i> Biochemical, behavioral, and molecular assays were employed to assess oxidative stress markers, enzyme activities, locomotor performance, cell viability, and gene expression. Sodium arsenite exposure significantly decreased acetylcholinesterase activity, total thiols, glutathione (GSH), glutathione-S-transferase (GST), and nitric oxide, while increasing hydrogen peroxide, lipid peroxidation, protein carbonyls, and metabolic hyperactivity. These alterations were effectively ameliorated by <i>T. globiferus</i> fractions, with the methanol and butanol fractions producing the most consistent improvements (<i>P</i> < 0.05). Behavioral assessment revealed that sodium arsenite reduced negative geotaxis performance to 39% climbing ability, which improved to 55% following butanol fraction treatment. Molecular analysis demonstrated that sodium arsenite suppressed <i>p53</i> and <i>SOD1</i> expression while inducing <i>Ras</i> and <i>CNcC</i> overexpression. Treatment with <i>T. globiferus</i> fractions restored <i>p53</i> and <i>SOD1</i> expression, suppressed <i>Ras</i> overexpression, and normalized <i>CNcC</i> transcription factor levels. These findings provide the in vivo evidence that <i>T. globiferus</i> mitigates arsenic-induced oxidative stress and genetic dysregulation through coordinated biochemical and transcriptional modulation. The dual ability to restore redox homeostasis and reprogram oncogenic signaling underscores its potential as a natural redox therapeutic against toxin-induced and carcinogenesis-linked pathologies.