Lim D J
Am J Otolaryngol. 1986 Mar-Apr;7(2):73-99. doi: 10.1016/s0196-0709(86)80037-0.
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.
本文综述了目前有关声创伤和氨基糖苷类耳毒性所涉及的细胞机制的信息，以期对可能与听觉器官功能损害相关的细胞事件有新的认识。根据现有数据，可对所涉及的细胞机制做出以下假设。1）静纤毛和表皮板的大分子破坏是声创伤中的初始细胞事件。这种破坏会影响转导过程的微力学，导致暂时阈移。进一步的细胞损伤将涉及细胞修复和存活所需的基本细胞功能，如蛋白质、脂质和葡萄糖合成，而这种损伤将导致永久性细胞损伤或细胞死亡，从而导致永久性阈移。2）可以推测，氨基糖苷类耳毒性所涉及的细胞机制包括两个事件。早期事件是毛细胞内淋巴侧转导通道的可逆性阻断。后期事件是由于氨基糖苷类与磷脂和/或蛋白质结合，干扰蛋白质和/或磷脂合成等细胞功能，导致细胞死亡。氨基糖苷类从毛细胞外淋巴侧的渗透或膜介导内化可能会促进后一事件的发生。
