Histochemical evaluation of ethanol extracts of Senecio biafrae leaves in mercury chloride-induced hepatic injury in adult male Wistar rats

Introduction and aim. Mercury chloride is a potent hepatotoxin that disrupts liver architecture, glucose metabolism, and nuclear integrity. To our knowledge, no previous study has evaluated the histochemical effects of the ethanol extract of Senecio biafrae leaves (EESBL) on mercury chloride-induced hepatic injury. This study presents new evidence for the glycogen stabilizing and genoprotective properties of its compounds. Material and methods. Forty-nine adult Wistar rats were randomly assigned to seven groups (n=7 per group). Except for the control, all received 4 mg/kg mercury chloride orally for 21 days. Group II rats were sacrificed immediately after exposure, while group III underwent a 21-day recovery. Group IV received 2 mg/kg silymarin, and also Groups V–VII received 200, 400, and 600 mg/kg EESBL, respectively, for 21 days. Liver tissues were harvested for histochemical evaluation using periodic acid-Schiff (PAS) and Feulgen staining. Results. Mercury chloride significantly depleted liver glycogen stores (PAS-positive area: control 75.00±0.56% vs toxic 20.00±1.09%). EESBL restored glycogen storage in a dose-dependent manner (200 mg/kg: 52.02±0.56%; 400 mg/kg: 60.00±0.57%; 600 mg/kg: 72.06±0.57%), approaching silymarin (68.00±0.57%). Nuclear DNA integrity was markedly affected by HgCl2 (Feulgen-positive area: control 16.20±0.19% vs toxic 9.00±0.33%). EESBL improved nuclear morphology and DNA intensity (200 mg/kg: 11.11±0.12%; 400 mg/kg: 13.20±0.44%; 600 mg/kg: 14.06±0.33%), comparable to silymarin (14.00±0.25%) (all p<0.001). Conclusion. EESBL demonstrated protective effects against mercury chloride-induced hepatotoxicity by stabilizing hepatic glycogen metabolism and nuclear structure, underscoring its therapeutic potential in mitigating heavy metal-induced liver injury.