Tapinanthus globiferus 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 Tapinanthus globiferus fractions (butanol, methanol, and ethyl acetate) on sodium arsenite-exposed Drosophila melanogaster. 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 T. globiferus fractions, with the methanol and butanol fractions producing the most consistent improvements (P < 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 p53 and SOD1 expression while inducing Ras and CNcC overexpression. Treatment with T. globiferus fractions restored p53 and SOD1 expression, suppressed Ras overexpression, and normalized CNcC transcription factor levels. These findings provide the in vivo evidence that T. globiferus 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.