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短暂的光化学诱导氧化损伤会导致晶状体不可逆损伤和白内障。II. 作用机制。

A brief photochemically induced oxidative insult causes irreversible lens damage and cataract. II. Mechanism of action.

作者信息

Spector A, Wang G M, Wang R R, Li W C, Kleiman N J

机构信息

Department of Ophthalmology, College of Physicians & Surgeons of Columbia University, New York, NY 10032, USA.

出版信息

Exp Eye Res. 1995 May;60(5):483-93. doi: 10.1016/s0014-4835(05)80063-6.

DOI:10.1016/s0014-4835(05)80063-6
PMID:7615014
Abstract

Using photochemically induced oxidative stress and rat lenses in organ culture with 4% O2 and 4 microM riboflavin, it has been found that the observed changes in lens parameters are, in most cases, irreversible. This has made possible the elucidation of the sequence of biological changes leading to cataract. The earliest detectable changes in lens cell biology are observed in the epithelial cell redox set point and at the DNA level in terms of DNA integrity and 3H-thymidine incorporation followed by decreased membrane transport and changes in gene expression. Significant modification in classical cataract parameters such as hydration, steady state non-protein thiol, glyceraldehyde-phosphate-dehydrogenase activity and transparency occur at later times. The data suggest a definitive pattern of lens breakdown resulting in opacity starting at the epithelial cell level and leading to subsequent fibre cell involvement.

摘要

利用光化学诱导的氧化应激以及在4%氧气和4微摩尔核黄素条件下进行器官培养的大鼠晶状体,已发现大多数情况下,所观察到的晶状体参数变化是不可逆的。这使得阐明导致白内障的生物变化序列成为可能。晶状体细胞生物学中最早可检测到的变化出现在上皮细胞氧化还原设定点以及DNA水平,涉及DNA完整性和3H-胸腺嘧啶掺入,随后是膜转运减少和基因表达变化。经典的白内障参数,如含水量、稳态非蛋白硫醇、甘油醛-3-磷酸脱氢酶活性和透明度,在后期会发生显著改变。数据表明晶状体破坏存在一种明确的模式,始于上皮细胞水平,导致透明度下降,随后累及纤维细胞。

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