Ohta Y, Yamasaki T, Niwa T, Goto H, Majima Y, Ishiguro I
Department of Biochemistry, School of Medicine, Fujita Health University, Toyoake, Japan.
Ophthalmic Res. 1999;31(5):321-31. doi: 10.1159/000055554.
We attempted to clarify the pattern of cataract development in 12-month-old rats fed a 25% galactose diet and to assess the relation of cataract development with osmotic stress and oxidative damage. In lenses of 12-month-old male Wistar rats fed a 25% galactose diet over an 8-month period, suture accentuation appeared at 6 months of galactose feeding and then opacities developed from the anterior subcapsular cortex toward the posterior subcapsular cortex, reaching the nuclear region at 8 months of galactose feeding. Increases in lens galactitol and lipid peroxide contents and a decrease in lens reduced glutathione content occurred at 4, 6 and 8 months of galactose feeding. The increase in lens lipid peroxide content and the decrease in lens reduced glutathione content were accelerated with an increase in feeding period, while the increase in lens galactitol content was decelerated. An increase in lens water content and a decrease in lens protein content occurred at 6 and 8 months of galactose feeding. The lens vitamin E content increased at 6 months of galactose feeding and this increase was concomitant with increases in serum vitamin E and total cholesterol concentrations. The serum lipid peroxide concentration increased at 4 and 6 months of galactose feeding. The present results indicate that in lenses of 12-month-old rats fed a 25% galactose diet, suture accentuation appears initially and then opacities develop from the anterior subcapsular cortex toward the posterior subcapsular cortex, finally reaching the nuclear region. These results also suggest that in the galactosemic aged rats, osmotic stress would mainly contribute to cataract formation, while oxidative damage could be linked to both cataract formation and progression, although an increase in lens vitamin E content occurs during the cataract development.
我们试图阐明喂食25%半乳糖饮食的12月龄大鼠白内障的发展模式,并评估白内障发展与渗透压应激和氧化损伤之间的关系。在8个月期间喂食25%半乳糖饮食的12月龄雄性Wistar大鼠的晶状体中,喂食半乳糖6个月时出现缝线加重,然后混浊从前囊下皮质向后囊下皮质发展,在喂食半乳糖8个月时到达核区。喂食半乳糖4、6和8个月时,晶状体半乳糖醇和脂质过氧化物含量增加,晶状体还原型谷胱甘肽含量降低。晶状体脂质过氧化物含量的增加和晶状体还原型谷胱甘肽含量的降低随着喂食时间的增加而加速,而晶状体半乳糖醇含量的增加则减速。喂食半乳糖6和8个月时,晶状体含水量增加,晶状体蛋白含量降低。喂食半乳糖6个月时,晶状体维生素E含量增加,这种增加与血清维生素E和总胆固醇浓度的增加同时出现。喂食半乳糖4和6个月时,血清脂质过氧化物浓度增加。目前的结果表明,在喂食25%半乳糖饮食的12月龄大鼠的晶状体中,最初出现缝线加重,然后混浊从前囊下皮质向后囊下皮质发展,最终到达核区。这些结果还表明,在患半乳糖血症的老年大鼠中,渗透压应激可能是白内障形成的主要原因,而氧化损伤可能与白内障的形成和进展都有关,尽管在白内障发展过程中晶状体维生素E含量会增加。