摘要
目的：探讨自由基在卡那霉素（ＫＭ）内耳中毒中的作用．方法：豚鼠６６只，分正常对照组、ＫＭ组、ＫＭ＋尼莫地平（ＮＤ）组、ＫＭ＋超氧化物岐化酶（ＳＯＤ）组．连续用药１２ｄ，停药４ｄ后，分别测试听性脑干反应（ＡＢＲ）阈移、血清ＳＯＤ和耳蜗组织丙二醛（ＭＤＡ），同时也对耳蜗组织作扫描电镜观察．结果：ＫＭ组ＡＢＲ阈移和耳蜗ＭＤＡ显著高于对照组、ＮＤ和ＳＯＤ组（Ｐ＜０．０１），其血清ＳＯＤ明显低于对照组（Ｐ＜０．０１），毛细胞严重损伤．ＮＤ和ＳＯＤ组耳蜗ＭＤＡ与对照组无明显差异（Ｐ＞０．０５），ＡＢＲ阈移仍较对照组高，且毛细胞有不同程度损伤．结论：ＫＭ内耳中毒有自由基作用。
Objective: To study the effects of free radical on kanamycin (KM) ototoxicity in the inner ear. Method: Sixty six guinea pigs were randomly divided into four groups: normal control; KM; KM+nimodipin (ND); KM+superoxide dismutase (SOD). The animals were given the above drugs for 12 d. Auditory brainstem response (ABR) hearing thresholds were measured before and after the experiment. After 4 d of stopping treatment, the MDA levels of cochlea tissues were assayed in the all animals except ten for scanning electron microscope observation. Serum SOD levels of the control and KM groups were measured at the same time. Results: The ABR hearing threshold and MDA levels of KM group were significantly higher than the other three groups ( P <0.01), but the serum SOD levels in KM group was obviously lower than the control group ( P <0.01). The hair cells were also severely damaged in KM group. The MDA level in the SOD and ND group were no significant difference from the control group ( P >0.05), but the ABR hearing thresholds of SOD and ND group were higher than the control group and the hair cells were also damaged in some extents. Conclusion: The results indicate that the KM ototoxicity may induce cochlea damages and hearing loss may involve the effect of free radicals. The SOD and ND partially prevent KM ototoxicity.
出处
《第四军医大学学报》
1996年第1期8-10,共3页
Journal of the Fourth Military Medical University
基金
国家自然科学基金资助项目
关键词
卡那霉素
耳毒性
自由基
豚鼠
kanamycin ototoxicity free radical lipid peroxidation superoxide dismutase
