Background and Objective: Cobalt is a metal with a significant hazard profile, used widely in many industries. The reported hazards of Cobalt include effects on the heart, thyroid, immune system, vision and hearing organs as a result of exposure to high doses. This study aimed to evaluate the biochemical and histopathological effect of taxifolin on Co-induced ototoxicity in rats. Materials and Methods: Distilled water was administered to the Healthy Group (HG) and cobalt-only (Co) groups of animals and a third group was orally given 50 mg kg(-1) Taxifolin+Cobalt (TCo) by gavage. After 1 hr, 150 mg kg(-1) CoCl2 was administered orally to the stomach by gavage to the animals in the TCo and the Co groups. This procedure was repeated once a day for seven days. Results: Malondialdehyde (MDA), Nuclear Factor-Kappa B (NF-kappa B), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) levels were significantly higher than the HG and TCo groups and the cochlear nerve tissue was damaged by significant histopathological damage in the Co group with low total glutathione (tGSH) levels. In the TCo group, biochemical and histopathological findings were found to be close to the HG group. Conclusion: This study revealed the role of oxidative stress and proinflammatory cytokines in the pathogenesis of Co ototoxicity. Our results suggest that taxifolin may be useful in the treatment of Co-related ototoxicity.