Effects of noise and ototoxic drugs at the cellular level in the cochlea: A review

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Currently available information concerning the cellular mechanisms involved in acoustic trauma and aminoglycoside ototoxicity is reviewed to shed some new light on the cellular events that may be related to functional impairment of the auditory organ. Based on the available data, the following postulations can be made concerning the cellular mechanisms involved. 1) The macromolecular disruption of the stereocilia and cuticular plates is the initial cellular event in acoustic trauma. This disruption would affect the micromechanics of the transduction process, leading to temporary threshold shift. Further cellular impairment would involve basic cellular functions such as the protein, lipid, and glucose synthesis needed for cell repair and survival, and such impairment would result in permanent cell injury or cell death, leading to permanent threshold shift. 2) It can be postulated that the cellular mechanisms involved in aminoglycoside ototoxicity include two events. The early event is the reversible blockage of the transduction channels from the endolymph side of the hair cells. The later event is the interference in such cellular functions as protein and/or phospholipid synthesis because of binding of aminoglycoside to the phospholipids and/or protein, leading to cell death. The latter event may be facilitated by penetration or membrane-mediated internalization of the aminoglycoside from the perilymph side of the hair cell.

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    This study was supported in part by a grant from the Deafness Research Foundation and contracts from the U.S. Air Force (Aerospace Medical Research Laboratory, Wright-Pat-terson Air Force Base) and the National Institute of Occupational Safety end Health.

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