Protective effect of ethyl pyruvate on amikacin-induced ototoxicity in rats

S Dedeoğlu1, M Ayral

  • 1Department of Otorhinolaryngology, Gazi Yasargil Training and Research Hospital, Diyarbakir, Turkey. drserkandedeoglu@gmail.com.

Abstract

Insights

Ethyl pyruvate (EP) protects against amikacin (AMK) induced ototoxicity. This study shows EP's antioxidant and anti-inflammatory properties mitigate AMK's harmful effects on hearing function.

Area of Science:

  • Ototoxicity research
  • Pharmacology
  • Biochemistry

Background:

  • Amikacin (AMK) is a vital antibiotic, but its use is restricted by ototoxic side effects.
  • Ethyl pyruvate (EP) possesses known antioxidant and anti-inflammatory properties.

Purpose of the Study:

  • To investigate the protective effects of ethyl pyruvate (EP) against amikacin (AMK) induced ototoxicity.
  • To evaluate the biochemical and functional changes associated with AMK ototoxicity and EP intervention.

Main Methods:

  • Wistar albino rats were administered AMK (600 mg/kg/day) or AMK + EP (50 mg/kg/day) for 14 days.
  • Auditory Brainstem Responses (ABR) and Distortion Product Otoacoustic Emissions (DPOAE) were assessed.
  • Biochemical markers of oxidative stress (TOS, OSI, MDA) and inflammation (TNF-α, IL-1β, IL-6) were analyzed.

Main Results:

  • Amikacin administration significantly impaired hearing function, increased oxidative stress markers (TOS, OSI, MDA), and elevated pro-inflammatory cytokines.
  • Ethyl pyruvate treatment significantly improved hearing function in the AMK+EP group.
  • EP intervention normalized oxidative stress markers and prevented the elevation of pro-inflammatory cytokines seen with AMK alone.

Conclusions:

  • Ethyl pyruvate demonstrates significant protective effects against amikacin-induced ototoxicity.
  • The protective mechanism of EP involves its potent antioxidant and anti-inflammatory actions.
  • EP represents a potential therapeutic agent to mitigate amikacin's ototoxic side effects.