Abstract: Lead toxicity remains a major public health concern due to its detrimental effects on vital organs, particularly the liver and kidneys. This study evaluated the protective effects of aqueous extracts of watermelon (Citrullus lanatus) seeds on hepatic and renal functions in lead-induced Wistar rats. A total of four experimental groups were used: a normal control, a lead-exposed group, and two treatment groups administered 200 mg/kg and 400 mg/kg of watermelon seed extract alongside lead exposure. Liver function markers: Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), and Alkaline Phosphatase (ALP) as well as renal biomarkers; urea and creatinine were assessed. Results showed that lead exposure significantly elevated AST, ALT, ALP, urea, and creatinine levels, indicating hepatic and renal damage. However, treatment with the aqueous watermelon seed extract produced a dose-dependent improvement. Notably, the 400 mg/kg dose significantly reduced ALP levels and restored AST and ALT values close to normal. Similarly, both treatment groups showed reductions in urea and creatinine levels, although these changes were not statistically significant. These findings suggest that aqueous watermelon seed extract possesses hepatoprotective and nephroprotective properties, likely due to its bioactive phytochemicals with antioxidant potential. The higher dose demonstrated greater efficacy, indicating a dose-dependent therapeutic effect. The findings suggest that the aqueous extract of C. lanatus seeds possesses protective and ameliorative effects against lead-induced hepatorenal dysfunction in male Wistar rats. This study highlights the potential of watermelon seed extract as a natural therapeutic for mitigating heavy-metal-induced hepatorenal toxicity, warranting further investigation into its mechanisms of action, safety profile, and potential translational applications in human hepatic and renal health.
Keywords: Lead toxicity; Citrullus lanatus seed aqueous extract; Renal biomarkers; Wistar rats; Dose-dependent effect