Hepatoprotective Effect of Morin Against Lead-Induced Oxidative Stress and Structural Alterations in Male Wistar Rats: An In Vivo and In Silico Approach.

Lead, a naturally occurring heavy metal contaminant, poses serious environmental and health risks. Upon exposure, it accumulates in various organs and disrupts normal physiological functions. In the liver, it induces oxidative stress by generating reactive oxygen species and impairing antioxidant defenses, leading to hepatotoxicity. Plant-derived antioxidants have shown considerable efficacy in mitigating such toxic effects. Therefore, this study evaluates the hepatoprotective potential of morin, a bioactive flavonoid, against lead-induced oxidative damage and structural alterations in male Wistar rats. Animals were allocated equally into four experimental groups: control, morin-treated (50 mg/kg b.wt), lead-exposed (30 mg/kg b.wt), and lead + morin co-treated group, which received respective doses intragastrically for 28 days. Results showed that morin significantly attenuated lead-induced hepatotoxicity as indicated by reduced lipid peroxidation and protein oxidation in biochemical assays. The FTIR analysis further confirmed oxidative modifications in lipid and protein structure, implying disruption of their molecular integrity due to lead exposure. Further, morin treatment considerably improved the activities of acetylcholinesterase, superoxide dismutase, and catalase, along with increased glutathione content in lead-exposed rats. The molecular docking analysis also revealed a strong binding affinity (-6.55 and -8.97 kcal/mol) of morin with superoxide dismutase and catalase, supporting its role in modulating antioxidant defense mechanisms. Morin also prevented lead-induced hepatic deformities, including hydropic degeneration, portal vein congestion, and extensive collagen fiber deposition, as demonstrated by the histological and electron microscopy examinations. Conclusively, this subchronic study highlights morin's therapeutic potential and antioxidative efficacy in the liver tissue of rats subjected to lead exposure.