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作 者:李冰[1] 李晋春[1] 王效武[1] 史静华[1] 葛京京[1] 赵佳慧[2] 赖积香[3]
机构地区:[1]山西省眼科医院,太原030002 [2]山西医科大学分子生物学教研室 [3]中国辐射防护研究所
出 处:《眼科研究》2005年第5期485-487,共3页Chinese Ophthalmic Research
基 金:山西省卫生厅攻关基金项目(2000157)
摘 要:目的研究不同波长紫外线照射所致兔角膜光损伤的发生机制。方法分别用265nm和300nm紫外线照射8只白色家兔角膜,分别在24h和76h后取角膜进行光镜、透射电镜检查和应用TUNEL技术进行DNA断端标记。结果265nm紫外线照射24h和76h后,TUNEL阳性染色仅见于上皮细胞层,300nm照射24h后,TUNEL阳性染色见于上皮细胞和基质层角膜细胞,透射电镜也证实了典型的凋亡现象,表现为细胞皱缩,染色质浓缩成团块,聚集于核膜,凋亡小体形成。未发现明显的炎性反应。结论细胞凋亡是紫外线照射后角膜细胞死亡的发生机制。300nm比265nm紫外线照射引起更广泛角膜基质损伤。Objective To study the mechanism of light damage induced by different wavelengths of ultraviolet (UV) radiation in rabbit corneas. Methods The corneas of eight white rabbit were exposed to 265nm and 300nm UV. Animals were killed 24 and 76 hours after UV exposure. Radiated corneas were processed for light and transmission electron microscopy(TEM) examinations. In situ end labeling of fragmented DNA was made by using a modification of the TUNEL technique. Results Corneas exposed to 265nm UV showed TUNEL-positive staining only in epithelial cells at 24 and 76 hours. Twenty-four hours after 300nm UVR exposure, TUNEL-positive staining was presented in the epithelial cells and keratocytes throughout the whole thickness of the stroma. Transmission electron microscopy verified the typical apoptosis, including cell shrinkage, condensation of chromatin into dense masses attached to the nuclear membrane and formation of apoptotic bodies. No signs of inflammation were found in any spacemen from radiated cornea. Conclusion Apoptosis appears to be a mechanism of corneal cell death after UV radiation. The 300nm UV radiation causes more extensive damage to the corneal stroma in comparison with 265nm UV radiation.
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