高功率微波辐射所致大鼠睾丸损伤的病理学研究

Pathological Study of Testicular Injury Induced by High Power Microwave Radiation in Rats

目的:探讨高功率微波(HPM)辐照后睾丸组织的病变特点、动态变化规律。方法:165只二级雄性W istar大鼠经0、3、10、30、100 mW/cm2HPM辐照5 m in,于照后6 h,1、3、7、14、28、90 d,采用光镜、电镜观察睾丸组织形态学及附睾精子畸形的变化。结果:3~100 mW/cm2HPM辐照均可引起大鼠睾丸生精细胞损伤,主要病变为生精细胞变性、坏死、脱落,多核巨细胞形成,精子减少,间质水肿。生精细胞损伤历经死亡脱落期、“空虚”期和再生修复期,具有局灶性、不均一性、阶段性等特点,且功率密度越大,病变越严重,3 mW/cm2辐照后1 d见散在生精小管生精细胞变性、坏死、脱落;10 mW/cm2辐照后6 h与3 mW/cm2辐照后1 d病变相似,但出现多核巨细胞;1~7 d时上述病变明显加重;30、100 mW/cm2辐照后6 h,不仅见生精小管生精细胞的变性、坏死脱落明显增加,还可见单个生精小管内灶性坏死及精子明显减少或缺失。在3 mW/cm2辐照后3 d,10 mW/cm2辐照后1~7 d,30、100 mW/cm2辐照后6 h^7 d附睾畸形精子率显著性增加(P<0.01或P<0.05)。结论:HPM辐照可引起大鼠睾丸生精细胞损伤,其损伤存在剂量效应和时间效应关系。

Objective： To explore the pathological characteristics and the dynamic change regularity of the testis induced by high pow- er microwave （HPM） radiation. Methods ： One hundred and sixty-five male Wistar rats were exposed to 0, 3, 10, 30 and 100 mW/cm^2 HPM radiation for five minutes, and changes of testicular morphology and teratogenic ratio of epididymal spermatozoa were observed through light microscope and electron microscope at 6 h, 1, 3, 7, 14, 28 and 90 d after radiation. Results ： Injury of testicular spermatogenic cells in rats might be induced by 3-100 mW/cm^2 HPM radiation, and the main pathological changes were degeneration, necrosis, shedding of spermatogenic cells, formation of muhinuclear giant cells, decrease or loss of sperm and interstitial edema. Injury of spermatogenic cells underwent such phases as death and shedding, cavitation, regeneration and repair, characterized by being focalized, inhomogenous and phased. And the severity of pathological changes of the testis increased with power density. There was only scattered degeneration, necrosis, shedding of spermatogenic cells in the seminiferous tubule one day after 3 mW/cm^2 radiation, and the pathological changes six hours after 10 mW/cm^2 radiation was similar to those one day after 3 mW/cm^2 radiation, but with the formation of muhinuclear giant cells, and the above-mentioned pathological changes aggravated from one day to seven days after radiation. There was a significant increase in degeneration, necrosis, shedding of spermatogenic cells, as well as a significant decrease in spermatozoa and focal necrosis in simple seminiferous tubules six hours after 30 and 100 mW/cm^2 radiation, and the subsequent changes were similar to those of 10 mW/cm^2 radiation. There was a significant increase in teratogenic ratio of epididymal spermatozoa at 3d, 1 -7d, 6 h-7 d after 3, 10, 30 and 100 mW/cm^2 microwave radiation respectively （ P〈0.01 or P〈0.05 ）. Conclusion ： HPM radiation may cause injury of testicular spermatogenic cells in rats, which has a positive correlation to radiation dosage and time.