Nephroprotective Effect of Citrus sinensis L. on Mercury Exposed Wistar Rats

Abstract

Context: Exposure to all forms of mercury has toxic effect on several biosystems. Disruption in structural, biochemical, and physiological renal integrity results in nephrotoxicity. Citrus sinensis L (sweet orange) has medicinal benefits for diverse ailments. Aim: This study evaluated the nephroprotective effect of ethanol fruit peel extract of C. sinensis (EPCS) against mercuric chloride (HgCl₂)‑ triggered nephrotoxicity in Wistar rats. Materials and Methods: Twenty‑five Wistar rats (150–180 g) were separated into five Groups (I‑V, n = 5): Group I received normal saline (1 ml/kg); Group II received HgCl₂ (5 mg/kg); Group III received reference drug, silymarin (100 mg/kg) + HgCl₂ (5mg/kg); Group IV received EPCS (750 mg/kg) + HgCl₂ (5 mg/kg); and Group V received EPCS (1250 mg/kg) + HgCl₂ (5 mg/kg). Treatments were for 14 days. Nephroprotective effect was evaluated using the biochemical assay for renal function, histological, and histochemical assessments using H and E and periodic acid Schiff (PAS) stains and quantification of PAS staining intensity using Imagej® NIH, US. Statistical Analysis Used: One‑way analysis of variance with Tukey post hoc test. Results: The results revealed remarkable (p < 0.05) alterations in renal functional biomarkers, especially urea, creatinine, and Na⁺ in HgCl₂-treated group compared to the controls. However, EPCS treatment ameliorated alterations comparable to the silymarin and control groups. Histological and histochemical examinations revealed severe distortions in renal histoarchitecture such as shrunken glomerulus and Bowman‑space dilatation for the rats exposed to HgCl₂ compared to controls. However, EPCS treatment ameliorated distortions by the preservation of renal histoarchitecture comparable to the silymarin and control groups. No remarkable difference for PAS staining intensity relative to controls. Conclusion: EPCS possesses potential nephroprotective effect against mercuric chloride‑induced toxicity in Wistar rats.