香烟烟雾暴露的大鼠晶状体白内障样改变中高度糖化终末产物及其相关荧光的研究

目的：通过检测在体暴露于香烟烟雾大鼠的晶状体中的高度糖化终末产物及其相关荧光，探讨香烟烟雾凝聚物在吸烟致大鼠晶状体白内障样改变中的可能作用机制。方法：雄性Wistar大鼠随机分2组，实验组每天暴露于香烟烟雾1h，连续90d，对照组大鼠只暴露于普通室内空气，其他条件相同。每只大鼠两只眼球在处死后摘除，一只做组织病理学检查，另一只用于研究体内糖化情况。荧光质谱仪检测激发吸收光370／440nm处高度糖化终末产物相关荧光，并通过HPLC检测N-羧甲基赖氨酸及pentosidine。结果：实验组晶状体上皮细胞发生显著组织形态学改变。如增生、肥大，上皮多层化，并有晶体上皮细胞移行于晶状体后囊，对照组未见上述改变。吸烟组晶体水溶性和非水溶性组分中高度糖化终末产物荧光和N-羧甲基赖氨酸及pentosidine显著升高。结论：香烟烟雾吸入致大鼠晶状体白内障样改变，伴随高度糖化终末产物形成，糖化是吸烟致白内障形成的一个可能机制。

Advanced Glycation End Products and Related Fluorescence in Lens Crystallins of Cigarette Smoke Exposured Rats

Objective: Our aims were to assess the significance of advanced glycation end products (AGEs) in cataractous changes in rat lens after in vivo cigarette smoke exposure,and to test whether glycation is the possible mechanism in smoke-related cataractogenesis. Methods:Male Wistar rats were randomized to 2 groups.Rats in group 1 wewe exposed to cigarette smoke for 1 hour each day for 90 consecutive days and rats in control group were exposed only to room air. Both eyes of all the animals were then enucleated and 1 eye prepared for histopathological examination, the other eye was used to study glycation in vivo. The AGEs were assayed with high-performance liquid chromatography (HPLC). Fluorescence was measured with excitation/emission 370/440nm on the fluorescence spectrophotometer. Results: Distinct histopathologic changes in the anterior lens epithelium, such as hyperplasia, hypertrophy, and epithelial multilayering, and the presence of swollen epithelial cells overlying the posterior lens capsule, were observed in the cigarette smoke exposured group, but not in the control group. Mean levels of fluorescence and the AGEs,N-Carboxymethyl-L-Lysine,and pentosidine were markedly elevated in water soluble and water insoluble fractions from cigarette smoke exposure group. Significant differences were observed betueen the water insoluble fractions and water sulable fractions.Conclusion:Cataractogenesis after cigarette smoke exposure in rats was associated with the formation of AGEs, and glycation may be the mechanism in smoke-related cataractogenesis.