Differential Amelioration of Aminoglycoside-Induced Oxidative Stress by Virgin Coconut Oil in the Vestibulocochlear Tissue and Serum of Wistar Rats

Abstract

Aminoglycoside (AG)-induced ototoxicity is primarily driven by the generation of reactive oxygen species (ROS) within the inner ear, leading to irreversible hair cell damage and death. Virgin coconut oil (VCO) is a natural product with potent antioxidant properties, but its specific effect on ROS levels within the vestibulocochlear tissue was unexplored. This study investigated the differential effects of VCO on concentrations of total ROS and inflammatory cytokine in the vestibulocochlear tissue and serum of rats treated with gentamicin (GTM). Thirty male Wistar rats were divided into six groups (n=5): normal control, GTM-only (80 mg/kg i.p.), GTM + Vitamin E (20 IU/kg, p.o.), and three GTM + VCO groups (1, 5, and 10 ml/kg, p.o.). Treatments were for 30 days, following which animals were sacrificed and serum and vestibulocochlear tissue homogenates were collected and assessed for total ROS, interleukin-1β (IL-1β), and tumor necrosis factor-alpha (TNF-α) using enzyme-linked immunosorbent assay (ELISA) kits. GTM treatment significantly elevated total ROS concentrations in both the vestibulocochlear tissue (146.02 ± 15.95 µg/mL) and serum (107.50 ± 1.29 µg/mL) compared to controls (tissue: 125.19 ± 2.68 µg/mL; serum: 87.49 ± 4.38 µg/mL; p < 0.05). Co-administration with VCO at all doses (1, 5, and 10 ml/kg) significantly reduced tissue ROS levels below control values (p < 0.05), with the 5 ml/kg dose being the most effective (83.59 ± 2.92 µg/mL). VCO was found to exert dose-dependent antioxidant effect on total ROS and TNF-α. These findings provide a biochemical basis for VCO's otoprotective effects al as a therapeutic adjuvant during AG therapy.