论文部分内容阅读
目的：通过对豚鼠实验性卡那霉素（ＫＭ）内耳中毒时血清及耳蜗外淋巴液中ＳＯＤ含量的检测，以探讨ＫＭ耳毒性内耳损伤自由基产生与可能的作用机制．方法：用放射免疫法和硫代巴比妥酸荧光法测定豚鼠实验性ＫＭ内耳中毒时血清和耳蜗外淋巴液中ＳＯＤ及耳蜗组织中丙二醛（ＭＤＡ）的含量，测定了内耳中毒前后脑干诱发电位（ＡＢＲ）阈移变化．结果：应用ＫＭ１２ｄＡＢＲ阈移明显增高的豚鼠ＭＤＡ含量也相应明显增高，而血清及外淋巴液中的ＳＯＤ则相反出现明显减少（Ｐ＜０．０１）．结论：ＫＭ听器损伤时血清及耳蜗组织中氧自由基反应增强可能是氨基糖甙类抗生素耳毒性听器损伤的因素之一．
OBJECTIVE: To explore the possible mechanism of free radical generation in the inner ear of KM ototoxicity induced by guinea pig kanamycin (KM) poisoning in the inner ear and the detection of SOD in serum and cochlear outer lymph. Methods: SOD and cochlear MDA contents in serum and cochlear extranodal fluid during guinea pig experimental KM inner ear poisoning were determined by radioimmunoassay and thiobarbituric acid fluorescence method. The contents of malondialdehyde Dry-evoked potential (ABR) threshold shift changes. Results: The content of MDA in guinea pigs with KM12dABR threshold increased obviously, while the SOD in serum and extranodal lymphocytes decreased significantly (P <0.01). CONCLUSION: The enhancement of oxygen free radical reaction in the serum and cochlea of KM rats may be one of the factors of the damage of aminoglycoside ototoxicity hearing aids.