Decades later, we still know relatively little about mechanisms through which these and
other compounds exert their ototoxic effects and about how to prevent them. We do know,
however, that a number of cellular responses are initiated following aminoglycoside
exposure. These include activation of multiple signaling cascades and ROS production, as
well as triggers of both necrotic and apoptotic-like cell death mechanisms [8, 9]. Despite
these generalities, it is clear that different classes of ototoxins stimulate hair cell death by
triggering different combinations of death-inducing pathways. For example, cisplatin
induces a number of different cellular responses when compared to aminoglycoside
antibiotics [9]. Even drugs within the same general class, (e.g., neomycin and gentamicin)
appear to act by different combinations of mechanisms [10]. The initiation of multiple
cellular processes following ototoxin exposure raises the possibility that many processes
could potentially be targeted alone or in combination to preserve hearing during treatment
with ototoxic drugs.