Ramamurthy_2026_J.Appl.Toxicol__

Auramine O (AO) is a widely used synthetic dye that poses serious environmental and health risks, yet the mechanisms underlying its multiorgan toxicity remain poorly understood. This investigation aims to assess the systemic toxicity of AO in Sprague-Dawley rats. The animals were divided into a control group, AO-exposed groups (5 and 10 mg/kg), and a positive control group receiving bisphenol A (50 mg/kg) for 90 days of exposure via oral gavage. Toxicity was assessed through body weight, serum biochemical markers, histopathology, gene expression (RT-PCR), immunohistochemistry, and HPLC-based quantification of AO in both urine and plasma. AO showed a quick systemic distribution to physiological organs and was primarily eliminated via the renal pathway. In addition, this study revealed a dose-dependent decrease in body weight. Biomarkers, such as bilirubin, albumin, glucose, creatinine, blood urea nitrogen (BUN), and creatine kinase levels, showed a significant elevation. In the brain homogenate, acetylcholinesterase level was notably reduced. Histopathological analysis of tissue samples revealed considerable damage to the liver (hepatic injury), kidney (tubular degeneration), heart (myocardial injury), and brain (neuronal degeneration). Gene expression analysis showed significant upregulation of inflammatory (tnf-alpha and nfkb) and apoptotic (caspase-3 and caspase-9) markers, and immunohistochemistry resulted in upregulated expression of nfkb. These results emphasize the potential health hazards linked to prolonged AO exposure, necessitating stringent environmental regulatory measures and further research into its long-term safety and potential therapeutic interventions.