Salicylate attenuates gentamicin-induced ototoxicity in the papilla basilaris of the lizard Podarcis sicula

It’s known that ototoxic side effects of gentamicin are caused by an iron-gentamicin complex that produces free radicals. Antioxidants attenuate gentamicin-induced free radical formation. We have previously demonstrated hair cell regeneration in both the crista ampullaris (organ involved in dynamic balance) and the saccule (organ involved in static balance) of gentamicintreated P. sicula. We now examine the fate of papilla basilaris (organ involved in hearing) hair cells after exposure to three doses of gentamicin. We want to determine whether there is any recovery and whether this is due to repair of damaged hair cells, to regeneration or, most likely, to both. In addition, we investigate whether antioxidants can effectively inhibit gentamicin-induced hair cell loss by SEM analysis using salicylate to protect against gentamicin ototoxic effects. Moreover, using BrdU, we tested whether or not there is hair cell regeneration following somministration of gentamicin. A BrdU immuno-fluorescence protocol was followed to detect BrdU-labelled cells. It was found that Gentamicin induced damage in the hair cells. Three days after the end of gentamicin treatment the hair cells of papilla showed fused or disarrayed stereovilli and there was widespread loss of hair cell bundles from the hair cells. Subsequently, numerous hair cells were lost. Conversely, when salicylate was co-administered with gentamicin the damage was moderated. The results suggest that administration of salicylate facilitates the recovery and reduces damage to hair cells after gentamicin treatment. Finally, we found evidence of bromodeoxyuridine incorporation initially in supporting cell nuclei and then in hair cell nuclei. This indicates that a process of sensory epithelium repair and hair cell regeneration occurred and that the recovery was due to both the proliferation of supporting cells and, as seems likely, selfrepair of hair cell bundles in weakly damaged sensory cells.