Effect of Aqueous Extract of Vernonia amygdalina on Renal Function in Wistar Albino Rats Exposed to Lead Toxicity

Abstract

Background: Lead exerts toxicity through multiple mechanisms, notably via the generation of reactive oxygen species (ROS), which induce oxidative stress, damage cellular structures, and impair antioxidant defense systems. Phytochemical analysis have identified several bioactive compounds in Vernonia amygdalina that could counteract lead-induced nephrotoxicity. Aim: This study aimed to investigate the potential protective effect of aqueous Vernonia amygdalina (Bitter leaf) extract (AVAE) on renal function in Wistar Albino rats exposed to lead toxicity. Methods: The leaves of V. amygdalina (bitter leaf) from five stations were screened for phytochemicals and heavy metals (lead, mercury, arsenic and cadmium) using thin layer chromatography and GBC XplorAA atomic absorption spectrophotometer. A total of Thirty-five (35) wistar albino rats were divided into five (5) groups of seven rats per group. Group I (Negative control) received normal saline only for 28 days, Group II (Positive control) were exposed to 50mg/kg lead acetate for 2 weeks and received no treatment throughout the study. Group III and IV were exposed to 50mg/kg lead acetate for 2 weeks and treated with AVAE at 2000mg/kg and 400mg/kg body weight (high and low dose respectively) orally for 28 days. Group V were not exposed to lead but treated with AVAE at a high dose, orally for 28 days. The experimental design included biomarkers of renal injury (Kidney Injury Molecule-1, Cystatin C), oxidative stress (DNA damage via 8-OHdG), and traditional renal function tests (urea and creatinine). Phytochemical analysis revealed the presence of bioactive compounds, including flavonoids, alkaloids, and saponins, while heavy metal analysis quantified contaminants in some of the plant samples. Acute toxicity studies confirmed the safety of AVAE up to 2000 mg/kg body weight. Results: The results from the study showed that Significant differences were observed between the groups (p < 0.05). Group II (positive control) showed the highest KIM-1, Cystatin C and DNA damage levels (indicative of severe kidney injury), while Groups III and IV (treated with high and low dose AVAE) showed significant reductions in KIM-1, Cystatin C and DNA damage levels with Group III (high dose AVAE) showing better response compared to Group II (Positive control), Group I and V which showed normal levels for all biomarkers. Elevated urea and creatinine in Group II indicated kidney dysfunction. AVAE treatment (Groups III and IV) reduced urea and creatinine levels, with high-dose treatment (Group III) providing the most significant improvement. Conclusion: Results demonstrated that AVAE significantly reduced oxidative stress, improved renal biomarkers, and mitigated kidney damage in lead-exposed rats, particularly at the high dose. These findings support the potential therapeutic role of Vernonia amygdalina in managing lead-induced nephrotoxicity. Future studies could explore its mechanisms of action and applicability in clinical settings to address heavy metal toxicity.