Abstract
Amikacin (AMK) is a widely used antibiotic, but its ototoxic side effects limit its use. This study investigated the effects of ethyl pyruvate (EP), known for its antioxidant and anti-inflammatory effects, against AMK ototoxicity. 32 Wistar albino rats (n: 8) were used in this study. To cause ototoxicity, AMK 600 mg/kg/day dose was applied intramuscularly for 14 days. EP was administered via ip at a dose of 50 mg/kg/day for 14 days. The Auditory Brainstem Responses (ABR) and Distortion Product Otoacoustic Emissions (DPOAE) tests were performed on the study's 0, 7, and 14 days. The results have shown that the hearing functions were significantly impaired with the AMK application. A significant improvement was observed in the AMK+EP group. While total oxidant status (TOS), oxidative stress index (OSI), and malondialdehyde (MDA) levels were found to be significantly higher in the AMK group compared to the control group, total antioxidant status (TAS) level was found to be significantly lower. In the AMK+EP group, on the other hand, deterioration in TOS, OSI, and MDA levels detected in the AMK group was not observed. No elevated pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6 were present in the EP+AMK group, which were detected in the AMK group. Hearing tests and biochemical results show that ethyl pyruvate has protective effects against amikacin ototoxicity due to its antioxidant and anti-inflammatory effects.
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