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目的探讨放疗后感音神经性耳聋的发生机制。方法将白化豚鼠94只随机分为观察组66只和对照组6只,观察组采用一次性70 Gy 60Co照射(右耳),于放疗后1、4、7、14、30 d各处死10只。对照组未进行放疗。取耳蜗中轴制作切片,HE染色观察结构变化,检测丙二醛(MDA)水平及超氧化物酶(SOD)活性;上述时间点分别取2只耳蜗基底膜行电镜扫描。结果放疗后观察组耳蜗出现不同程度损伤,观察组耳蜗MDA水平明显高于、SOD活性明显低于对照组,P均<0.01。结论放疗引起的耳蜗细胞损伤及MDA升高、SOD下降,此为感音神经性耳聋的发生机制。
Objective To investigate the mechanism of sensorineural deafness after radiotherapy. Methods A total of 94 albino guinea pigs were randomly divided into observation group (66) and control group (6). In the observation group, 70 Gy 60Co irradiation (right ear) . The control group did not radiotherapy. The central axis of the cochlear was sectioned and the changes of the structure were observed by HE staining. The levels of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) were detected. Two cochlear basilar membranes were taken under the scanning electron microscope. Results The cochlea of the observation group showed different degrees of injury after radiotherapy. The content of MDA in the cochlea in the observation group was significantly higher than that in the control group, P <0.01. Conclusion Radiation-induced cochlear cell injury and MDA increased, SOD decreased, which is the pathogenesis of sensorineural deafness.