Abstract
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. 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. 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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