DOSE-RELATED AMELIORATIVE EFFECTS OF COCONUT WATER (COCOS NUCIFERA L.) ON DOXORUBICIN-INDUCED RENAL INJURY IN MALE WISTAR RATS: BIOCHEMICAL AND HISTOPATHOLOGICAL EVIDENCE

Abstract

Doxorubicin is an effective anthracycline whose clinical use is limited by organ toxicity, including nephrotoxicity involving oxidative and nitrosative stress, inflammation and tissue remodelling. Coconut water (Cocos nucifera L.) contains antioxidant constituents, but evidence of its effects on doxorubicin-induced renal injury is limited. Forty-eight male Wistar rats were initially assigned to six groups (n = 8 per group): control; doxorubicin (DOX, 10 mg/kg, single intraperitoneal dose); DOX plus coconut water (6 or 12 mL/kg); and coconut water alone (6 or 12 mL/kg). During the seven-day experimental period, 12 animals died in the doxorubicin-containing groups. From the surviving animals, four rats were randomly selected per group for the final biochemical and histopathological analyses (n = 4 per group; total analysed = 24). Coconut water was administered orally once daily for seven days. Serum nitric oxide (NO), superoxide dismutase (SOD), kidney injury molecule-1 (KIM-1) and transforming growth factor-β1 (TGF-β1) were measured, and kidney sections were examined histologically. Doxorubicin increased NO and TGF-β1 and caused moderate histological injury among surviving animals, but did not increase KIM-1 or deplete SOD. Coconut water produced graded histological improvement, reaching near-normal architecture at 12 mL/kg, with dose-related NO reduction. TGF-β1 remained elevated in the co-treated groups. ANOVA showed significant group differences for NO, SOD, KIM-1 and TGF-β1 (p ≤ 0.0155), and TGF-β1 correlated strongly with NO (r = 0.716, p < 0.0001). Coconut water produced partial, dose-related amelioration of doxorubicin-associated renal injury, strongest at 12 mL/kg.