摘要
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 explore the mechanism of sensorineural hearing loss after irradiation. Methods Sixty-six guinea pigs were randomly divided into observed group(60 guinea pigs) and control group(6 guinea pigs). The right ears of observed group were given irradiation, 10 guinea pigs were sacrificed at I, 4, 7, 14 and 30 days after irradiation. The control group was given no irradiation. The specimens were dehydrated, embeded in paraffin and serially cutted. Sections were stained with haematoxylin and eosin for light microscopic examination, and the level of malondialdehyde (MDA) and activity of supperoxide dismutase (SOD) were examined. Results Inner ear damage was found in the observed group after irradiation, the level of MDA in observed group was significantly higher than that in control group, but the activity of SOD was significantly lower than that in control group. Conclusions Irradiation might cause cochlear cell damage, increse of MDA and decrease of SOD; this may be the mechanism of sensorineural hearing loss.
出处
《山东医药》
CAS
北大核心
2011年第35期31-33,共3页
Shandong Medical Journal
基金
广西壮族自治区自然科学基金资助项目(桂科字0832126)
关键词
放射治疗
神经性耳聋
丙二醛
超氧化物酶
耳蜗
irradiation
sensorineural hearing loss
malondialdehyde
supperoxide dismutase
inner ear