Cisplatin is widely used for the treatment of a number of solid malignant
tumors. However,
ototoxicity induced by
cisplatin is an obstacle to effective treatment of
tumors. The basis for this toxicity has not been fully elucidated. It is generally accepted that
hearing loss is due to excessive production of
reactive oxygen species by cells of the cochlea. In addition, recent data suggest that
inflammation may trigger inner ear cell death through endoplasmic reticulum stress, autophagy, and necroptosis, which induce apoptosis. Strategies have been extensively explored by which to prevent, alleviate, and treat
cisplatin-induced
ototoxicity, which minimize interference with antitumor activity. Of these strategies, none have been approved by the Federal Drug Administration, although several preclinical studies have been promising. This review highlights recent strategies that reduce
cisplatin-induced
ototoxicity. The focus of this review is to identify candidate agents as novel molecular targets,
drug administration routes, delivery systems, and dosage schedules. Animal models of
cisplatin ototoxicity are described that have been used to evaluate drug efficacy and side effect prevention. Finally, clinical reports of otoprotection in patients treated with
cisplatin are highlighted. For the future, high-quality studies are required to provide reliable data regarding the safety and effectiveness of pharmacological interventions that reduce
cisplatin-induced
ototoxicity.