Background: High doses of acetylsalicylic acid (ASS) induce tinnitus and hearing loss. This ototoxic side effect of ASS is characterized by a decrease in spontaneous and evoked otoacoustic emissions. A decrease in otoacoustic emissions is found not only in mammals, but also in non-mammalian ears without electromotile outer hair cells. The molecular mechanism underlying ASS ototoxicity seems to be competitive binding to and a block of the motor molecule prestin. In non-mammalian species, ASS ototoxicity is possibly explained by an effect on the hair bundle.
Results: The present data from the outer hair cells of the adult guinea pig cochlea show a reduction in the membrane capacitance by maximally 42%, probably as a result of ASS binding competitively to the motor molecule. However, spontaneous and evoked receptor currents were not modulated by ASS.
Conclusion: The results suggest an influence of ASS on outer hair cell somatic electromotility, without a concomitant effect on hair-bundle function.
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