Experimental animal models of drug-induced sensorineural hearing loss: a narrative review

Abstract

This narrative review describes experimental animal models of sensorineural hearing loss (SNHL) caused by ototoxic agents.Background: SNHL primarily results from damage to the sensory organ within the inner ear or the vestibulocochlear nerve (cranial nerve VIII). The main etiology of SNHL includes genetic diseases, presbycusis, ototoxic agents, infection, and noise exposure. Animal models with functional and anatomic damage to the sensory organ within the inner ear or the vestibulocochlear nerve mimicking the damage seen in humans are employed to explore the mechanism and potential treatment of SNHL. These animal models of SNHL are commonly established using ototoxic agents.Methods: A literature search of PubMed, Embase, and Web of Science was performed for research articles on hearing loss and ototoxic agents in animal models of hearing loss.Conclusions: Common ototoxic medications such as aminoglycoside antibiotics (AABs) and platinum antitumor drugs are extensively used to induce SNHL in experimental animals. The effect of ototoxic agents in vivo is influenced by the chemical mechanisms of the ototoxic agents, the species of animal, routes of administration of the ototoxic agents, and the dosage of ototoxic agents. Animal models of drug-induced SNHL contribute to understanding the hearing mechanism and reveal the function of different parts of the auditory system in humans.

Exploring the effects and mechanisms of organophosphorus pesticide exposure and hearing loss

“…Similar to the ototoxicity of aminoglycoside antibiotics and cisplatin, OP exposure resulted in morphological alterations in cochlea, threshold elevation, and prolongation of the interpeak latencies. However, the effects of OPs-induced hearing loss on experimental animals may be affected by animal species, dose, duration, and delivery route of agents (98). The exposure route in animal experiments could be different in humans, leading to an inconsistent outcome.…”

The audiological characteristics of infant auditory neuropathy patients without otoacoustic emission

“…As such, the possible mechanism that can explain the reason of OAE absent but CM can be recorded are as follow: (a) OAE is more sensitive to the damage of OHCs 12 . Previous studies have shown that DPOAE has changed before the change of CM when no obvious structural change is found by electron microscopy 16,17 . When the OHCs have a certain degree of damage, OAE cannot be elicited but CM can be elicited.…”

“… 12 Previous studies have shown that DPOAE has changed before the change of CM when no obvious structural change is found by electron microscopy. 16 , 17 When the OHCs have a certain degree of damage, OAE cannot be elicited but CM can be elicited. CM may be derived from residual OHCs and IHCs, as the function of IHCs may be preserved when the lesion site of AN is synapse or postsynaptic, although its contribution to CM is minimal (15%–20%).…”

Advancements in prevention and intervention of sensorineural hearing loss

“…Moreover, other ototoxic drugs including doxorubicin (DOXO), aromatic solvent, ouabain, glutamic acid, glutamate analogues, 2-hydroxypropyl-β-cyclodextrin (HPβCD), and heavy metals also contribute to ototoxic drug–induced SNHL. 33 Kyle et al 34 reported that aspirin has a dose-dependent ototoxic side effect in elderly people, but the damage is reversible. Sensory hair cells undergo necroptosis and apoptosis after exposure to ototoxic drugs.…”