| Objective: Wind tunnel noise was simulated according to acoustics data collectedon-site to establish noise-induced deafness model in mice and investigate the damage ofauditory brainstem response (ABR) and cochlear ultrastructure. Estrogen wasadministrated to the mice after they were departed from wind tunnel noise and changesof ABR and cochlear ultrastructure were observed. Based on the data observed, weexplored the protective effects of estrogen on noise-induced hearing loss so as toprovide basic evidence for the prevention and treatment of noise-induced hearingdamage.Methods:40Kunming mice （male）were randomly divided into simple noise group（group A）and estrogen treatment group （group B）.All the mice were exposed towind tunnel noise8hours per day for7consecutive days. For group B, each mouse wasgiven intramuscular injection of0.15mg estradiol benzoate30mins after the exposure.For group A, no treatment was performed. ABR thresholds were tested for each mouseat the point of pre-exposure; day3and7during the exposure; and days3and7after theexposure respectively.At the time of day7during the exposure and day7after theexposure,the mice were executed and treated in2.5%glutaraldehyde fixative in vitroand then fixed in the fixative for4hours after the cochleae were removed. Electronmicroscope observation included:(1) the mice cochleae were observed andphotographed by scanning electron microscope（SEM） after they were exposed thebasement membrane of hard-stripping method and were treated for dewatering, drying,gold processing,etc.(2) the mice cochleae were observed and photographed bytransmission electron microscope （TEM）after the specimens were immersed in10%EDTA to have a decalcification for three weeks and were treated for dehydration, embedding, curing, slicing and coloring.Results：There was no significant difference between the groups before the experiment.ABR thresholds of the two groups got raised after the exposure to wind tunnel noise andelevated with the accumulation of noise exposure.At the time of day3and7during theexposure,ABR thresholds of the two groups were higher than that before theexperiment, with no significant difference between the two groups. After the exposure,the ABR thresholds of the two groups shew different degrees of recovery. At the time ofday3and7after the exposure,ABR thresholds of group B were lower than that ofgroup A and there was significant difference between the two groups.Scanning electron microscopy showed the following changes: at day7exposure, themice cochleae suffered serious damage in both groups, with the inner and outer haircells(IHC and OHC) missing of sheet extensively and the Corti’s organ collapsing andcrimpling. After7days off the noise,the IHC and OHC of group A had a small limitedpunctate missing and the Corti’s organ collapsed, crimpled and deformed.The damageof cochleae of the group B was lighter with only a mild IHC confused and merged, andthe OHC were normal in the main.Transmission electron microscopy showed the following changes: after the noiseexposure of7days for the two groups,there were many vacuoles in the IHC and OHC,and the number of mitochondria decreased. After the noise exposure of7days, themitochondrion of OHC were generally normal with almost no vacuole in group A.Athough there were vacuoles in IHC, they were lower than that of noise exposure of7days.There were a few vacuoles in the cytoplasm of IHC in group B, and themitochondrion were normal and no vacuole existed.Conclusion：Wind tunnel noise could lead to the raise of ABR thresholds with theaccumulation of noise exposure. After the exposure, the hearing of the two groups haddifferent degrees of recovery and the recovery of group B was better than that of groupA. Wind tunnel noise could also cause cochlear damage in mice and the injury of groupB was lighter than that of group A.The damage of cochlear ultrastructure was inaccordance with the changes of hearing loss.Estrogen appeared to protect againstnoise-induced hearing loss. |
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