Toxicological assessment of thyroid disruption caused by benzoyl peroxide in Wistar rats

Benzoyl peroxide (BPO) is a widely utilized ingredient in medicinal and cosmetic products. This 21day sub-chronic research evaluated the systemic toxicological effects of oral BPO administration at two dose levels (50 and 100mg/kgbw) in experimental rats. Endpoints including hepatic oxidative stress indicators (SOD, CAT, GST, MDA, and GSH), serum liver function enzymes (SGPT, SGOT, and ALP), tissue histology, and hormone profiling (T3, T4, TSH) were examined to assess the Hypothalamic-Pituitary-Thyroid (HPT) axis. Molecular docking evaluated BPO’s binding affinity to thyroid hormone receptors (TR1α and TR1β). Significant dose-dependent increases in serum ALP corroborated BPO-induced hepatotoxicity, though SGPT levels showed no significant changes. Increased antioxidant enzymes and decreased GSH indicated marked hepatic oxidative stress. Endocrine findings indicated primary hypothyroidism, with elevated TSH and reduced T3 and T4, supported by histopathological alterations in thyroid tissue. Lastly, the in silico investigation showed binding affinity between BPO and both TR1α and TR1β. These findings suggest a dual-mechanism model of BPO toxicity involving systemic oxidative damage and putative direct molecular interference with thyroid hormone signaling, indicating BPO may act as a systemic toxicant that impairs the HPT axis.