Vrensen G, Kappelhof J, Willekens B
Department of Morphology, The Netherlands Ophthalmic Research Institute, Amsterdam.
Lens Eye Toxic Res. 1990;7(1):1-30.
Clear human post mortem lenses, varying in age between 23 and 82 years, were investigated using scanning and transmission electron microscopy. The lenses were obtained from the Corneabank Amsterdam. The post mortem delay ranged from 8-24 hours. Apart from some minor mitochondrial changes no hypoxic post mortem disturbances in epithelial cells and lens fibers were observed. In the lens fibers three main age-related fine structural alterations were found: i) membrane ruptures, ii) watervacuoles and iii) multilamellar bodies. The frequency of these alterations increased with age and they remained restricted to the superficial equatorial cortex. They were absent in the anterior and posterior cortex, supranuclear equatorial cortex and nucleus. The relevance of these observations in relation to the etiology and early pathogenesis of senile cataract is discussed. The membrane ruptures and watervacuoles are in morphological support of the view, based on biochemical evidence, that oxidative stress leads to destabilization and desintegration of membranes and consequently disturbs the waterbalance of fibers. It is postulated that the lamellar bodies are involved in the repair of ruptured membranes and breakdown of affected proteins thus explaining the late onset of senile cataractous changes.
利用扫描电子显微镜和透射电子显微镜对年龄在23至82岁之间的人类死后透明晶状体进行了研究。这些晶状体取自阿姆斯特丹角膜库。死后延迟时间为8至24小时。除了一些轻微的线粒体变化外,未观察到上皮细胞和晶状体纤维存在缺氧性死后干扰。在晶状体纤维中发现了三种主要的与年龄相关的细微结构改变:i)膜破裂,ii)水泡,iii)多层体。这些改变的频率随年龄增加而增加,且它们仅局限于赤道表面皮质。在前皮质、后皮质、赤道核上皮质和核中均未出现。讨论了这些观察结果与老年性白内障的病因和早期发病机制的相关性。基于生化证据,膜破裂和水泡在形态学上支持了氧化应激导致膜不稳定和解体从而扰乱纤维水平衡这一观点。据推测,多层体参与了破裂膜的修复和受影响蛋白质的分解,从而解释了老年性白内障变化的晚期发生。