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目的观察大鼠视网膜光化学损伤的主要组织化学改变。方法对动物模型进行视网膜超微结构观察、丙二醛含量测定、细胞色素氧化酶及镁激活三磷酸腺苷酶活性的组织化学观察。结果超微结构发现光照后６小时，光感受器细胞核肿胀，内节线粒体肿胀，外节水肿，视网膜色素上皮（ｒｅｔｉｎａｌｐｉｇｍｅｎｔｅｐｉｔｈｅｌｉｔｉｓ，ＲＰＥ）顶端微绒毛消失，溶酶体增多，６天反应加重。１４天光感受器细胞及内节已基本正常，外节再生但盘膜排列稀疏，ＲＰＥ顶端出现微绒毛。观察到光照后６小时及６天，视网膜细胞色素氧化酶及镁激活三磷酸腺苷酶活性下降，丙二醛含量增高，至１４天均有所恢复。结论脂质过氧化使光感受器细胞膜系统损伤崩解，引起细胞超微结构及酶活性改变，可能与视网膜光化学损伤的发病有关。
Objective To observe the major histochemical changes of retinal photochemical damage in rats. Methods The animal model was observed by ultrastructure of the retina, the content of malondialdehyde, cytochrome oxidase and magnesium activated adenosine triphosphatase activity were observed. Results Ultrastructure revealed that at 6 hours after light exposure, the nucleus of photoreceptors were swollen, mitochondria swollen, edema of outer segment, disappearance of microvilli at the top of retinal pigment epithelium (RPE), increased lysosomes and aggravated reaction on 6th day. 14 day photoreceptor cells and internal sections have been normal, external regeneration, but the disc is arranged sparsely, RPE top microvilli. Retinal cytochrome oxidase and magnesium-activated adenosine triphosphatase activity decreased and MDA content increased after 6 and 6 days of light exposure, respectively, and recovered to 14 days. Conclusion Lipid peroxidation damages the cell membrane of photoreceptor cells and causes changes of cell ultrastructure and enzyme activity, which may be related to the pathogenesis of retinal photochemical damage.