Abstract

Bisphenol-A (BPA), a common environmental contaminant, is linked to kidney toxicity through 
mechanisms involving inflammation and oxidative stress. Hesperidin, a bioactive compound 
found in citrus fruits, exhibits antioxidant and anti-inflammatory properties. This study 
investigated the protective role of hesperidin against BPA-induced renal damage. Thirty (30) male 
Wistar rats were randomly divided into six groups (n=5). Group A served as the normal control. 
Group B received 50  mg/kgBPA orally for 14 days. Groups C, D, and E were pre-treated with 
hesperidin at 50 mg/kg, 100 mg/kg, and 200 mg/kg, respectively, for 14 days, followed by BPA 
for another 14 days. Group F received 200  mg/kghesperidin alone for 28 days. After the treatment 
period, kidney and blood samples were collected for biochemical and histological assessments. 
Data analysis was performed using one-way ANOVA with Tukey’s post hoc test (p < 0.05). BPA 
administration significantly increased (p < 0.05) pro-inflammatory markers (IL-6, TNF-α), 
malondialdehyde (MDA), and serum levels of creatinine, urea, and uric acid, while antioxidant 
enzymes (SOD, Catalase, GPx) were reduced. Histological analysis revealed structural kidney 
damage in the BPA group. Hesperidin treatment significantly reversed these effects, showing 
reductions in inflammation and oxidative stress, along with improved kidney histology and 
function. These results suggest that hesperidin provides protective effects against BPA-induced 
renal toxicity by mitigating oxidative stress and inflammation and preserving kidney function. 
Keywords: Hesperidin, Bisphenol A (BPA), Oxidative stress markers, Kidney Toxicity, 
Inflammation.