Goto H, Yamakawa N, Hasemi M, Matsuura G, Usui M
Department of Opthalmology, Tokyo Medical College, Japan.
Nippon Ganka Gakkai Zasshi. 1994 Oct;98(10):1019-26.
The presence of superoxide generated by polymorphonuclear leukocytes (PMNs) was demonstrated in an experimental autoimmune uveoretinitis (EAU) model. Histopathological examination of the eyes, enucleated sequentially after the onset of EAU, and determination of retinal lipid peroxidation (LPO) revealed an increase in LPO products with progressive retinal tissue damage. In addition, histopathological changes, predominantly degeneration of the retinal outer segments, and increased retinal LPO were confirmed in vitro by culturing naive neural retina with activated PMNs. This increased LPO was inhibited by superoxide dismutase (SOD). These data suggest that lipid peroxidation reaction involving superoxide may play an important role in the pathogenesis of retinal tissue damage in ocular inflammatory disease characterized by the infiltration of PMNs.
在实验性自身免疫性葡萄膜视网膜炎(EAU)模型中证实了多形核白细胞(PMN)产生的超氧化物的存在。对EAU发病后依次摘除的眼睛进行组织病理学检查,并测定视网膜脂质过氧化(LPO),结果显示随着视网膜组织损伤的进展,LPO产物增加。此外,通过将未活化的神经视网膜与活化的PMN共同培养,在体外证实了主要为视网膜外段变性的组织病理学变化以及视网膜LPO增加。超氧化物歧化酶(SOD)可抑制这种增加的LPO。这些数据表明,涉及超氧化物的脂质过氧化反应可能在以PMN浸润为特征的眼部炎症性疾病的视网膜组织损伤发病机制中起重要作用。