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将豚鼠随机分为３组，第１组为庆大霉素（ＧＭ）组，１３只，第２组为生理盐水组，１０只， 第３组为正常对照组，１３只，检测各组动物耳蜗听功能、扫描电镜观察和测定耳蜗和血清中脂质过 氧化（ＬＰＯ）产物丙二醛（ＭＤＡ）含量的变化。结果表明ＧＭ组动物耳蜗神经动作电位（ＡＰ）阈值较 生理盐水组及正常组明显为高（Ｐ＜０．００１），ＡＰ（Ｎ１）潜伏期ＧＭ组较生理盐水组及正常组显著延 长（Ｐ＜０．０１），耳蜗扫描电镜显示ＧＭ组动物毛细胞受损程度同其听功能改变呈一致性。耳蜗中 ＭＤＡ检测结果表明，ＧＭ组耳蜗中ＭＤＡ含量较生理盐水组及正常组明显为高（Ｐ＜０．０１）。提示自 由基引起耳蜗ＬＰＯ可能是ＧＭ耳毒性机制之一。
The guinea pigs were randomly divided into three groups: the first group was gentamicin (GM) group, 13 rats, the second group was saline group, 10 rats, the third group was normal control group and 13 rats. Cochlear hearing function, scanning electron microscopy and determination of cochlear and serum lipid peroxidation (LPO) product malondialdehyde (MDA) content changes. The results showed that the threshold value of nerve action potential (AP) of cochlear nerve in GM group was significantly higher than that in normal saline group and normal group (P <0.001), and the latency of AP (N1) group was significantly longer than that in normal saline group and normal group (P < 0.01). The cochlear scanning electron microscopy showed that the damage of hair cells in GM group was consistent with the change of hearing function. The result of MDA in cochlea showed that the content of MDA in the cochlea of GM group was significantly higher than that in normal saline group and normal group (P <0.01). Tip free radical induced cochlear LPO may be one of the mechanisms of ototoxicity.