Avunduk A M, Yardimci S, Avunduk M C, Kurnaz L, Koçkar M C
Karadeniz Technical University, School of Medicine, Department of Ophthalmology, Trabzon, Turkey.
Exp Eye Res. 1997 Sep;65(3):417-23. doi: 10.1006/exer.1997.0344.
Cigarette smoking has been implicated in the pathogenesis of cataract, but the pathogenic mechanism by which cigarette smoke causes cataract is yet to be completely understood. There has been suggestion that oxidative damage caused by accumulation of Fenton reagents (iron and copper) in the lens can cause lens damage and possibly cataract. To investigate the accuracy of this theory the study was planned. A number of twenty-four male Wistar rats were divided randomly into experimental and control groups. The experimental group of rats were exposed to cigarette smoke for two hours in each day over sixty consecutive days and the controls were treated in identical fashion but only exposed to room air. At the end of the study period, both eyes of all the animals were enucleated and one eye prepared for histopathological examination and the other used for the measurement of metal levels. The lenses of experimental animals showed significantly decreased zinc and increased iron, and calcium concentration relative to those of sham exposed controls. However, no significant difference was found in the copper contents of the lenses of both groups. Distinct histopathological changes such as hyperplasia, hypertrophia, and multilayering of epithelial cells and elevations of calcium concentration detected in the lenses of experimental group animals suggested that the lens damage was a result of in-vivo exposure to tobacco smoke. We propose that increased metal contents in the lens can cause lens damage by the mechanism of oxidative stress through formation of oxygen radicals via metal catalysed Fenton reaction.
吸烟与白内障的发病机制有关，但香烟烟雾导致白内障的致病机制尚未完全明确。有人提出，晶状体中芬顿试剂（铁和铜）积累引起的氧化损伤会导致晶状体损伤，甚至可能引发白内障。为了研究这一理论的准确性，我们开展了此项研究。将24只雄性Wistar大鼠随机分为实验组和对照组。实验组大鼠连续60天每天暴露于香烟烟雾中2小时，对照组大鼠接受相同方式的处理，但仅暴露于室内空气中。在研究期结束时，摘除所有动物的双眼，一只眼睛用于组织病理学检查，另一只眼睛用于测量金属含量。与假暴露对照组相比，实验组动物晶状体中的锌含量显著降低，铁和钙浓度升高。然而，两组晶状体中的铜含量没有显著差异。实验组动物晶状体中检测到的明显组织病理学变化，如上皮细胞增生、肥大、多层化以及钙浓度升高，表明晶状体损伤是体内暴露于烟草烟雾的结果。我们认为，晶状体中金属含量的增加可通过金属催化芬顿反应形成氧自由基，以氧化应激机制导致晶状体损伤。
