Objective: This study aimed to explore whether carvacrol (CV) had a protective effect on paclitaxel-induced ototoxicity from biochemical, functional, and histopathological perspectives. Methods: Forty Wistar albino male rats were randomly separated into five groups of eight rats. Group 1 was the control group, so Paclitaxel or CV was not administered. Group 2 was administered i.p. CV at 25 mg/kg once a week; Group 3, was administered i.p. paclitaxel at 5 mg/kg once a week; Group 4 was administered i.p. paclitaxel at 5 mg/kg followed (30 min later) by CV at 25 mg/kg once a week; and Group 5 was administered i.p. CV at 25 mg/kg followed (1 day later) by paclitaxel at 5 mg/kg. once a week. The drugs were administered intraperitoneally once a week for four consecutive weeks, and distortion product otoacoustic emissions (DPOAE) tests were performed at the beginning of the study before the first drug administration and at the end of the study after the last drug administration. All rats were sacrificed, and cochleae were removed for biochemical and histopathological analysis. Results: Biochemical data indicated that paclitaxel caused oxidative stress in the cochlea. Histopathological findings revealed the loss of outer hair cells in the organ of Corti (CO) and moderate degenerative changes in the stria vascularis (SV). It was observed that DPOAE measurements were significantly reduced at high frequencies. In groups which CV was administered together with paclitaxel, these biochemical, histopathological, and functional changes were favorably reversed. Conclusion: CV may have a protective effect against paclitaxel-induced ototoxicity when given.