Yilmaz G, Turan B, Celebi N, Yilmaz N, Demirel Yilmaz E
Department of Ophthalmology, Başkent University School of Medicine, Başkent, Turkey.
Curr Eye Res. 2000 Jun;20(6):454-61.
To determine the effects of amiloride on selenite-induced cataracts, to identify this agent's role as an anti-oxidant, and to study related effects on ion levels in the rat lens.
Wistar albino rat pups were assigned to one of three groups, one control and two experimental. The first experimental group (Group 1; n = 22) received a subcutaneous injection of sodium selenite (30 nmol/g body weight) on postpartum day 10. The second experimental group (Group 2; n = 21) received a subcutaneous injection of amiloride (1 nmol/g body weight) 15 minutes before the sodium selenite injection. The control group (n = 22) received no injection. The pups in each group were observed during three weeks after the injection date. At the end of this period, the stage of cataract development was identified by comparison with slit lamp photographs and then the pups were sacrificed and their lenses were removed intracapsularly using a posterior approach. Cation analysis was carried out and glutathione and malondialdehyde levels were measured for each group.
Cataract stage in Group 1 was significantly higher than Group 2. Mean cataract stages in Groups 1 and 2 were 3.8+/-0.12 and 1.6+/-0.25 respectively. None of the control animals developed cataracts. Amiloride-pretreated group contained significantly higher glutathione levels than Group 1. The level of malondialdehyde in Group 1 lenses was approximately twice that in the lenses of the Group 2 amiloride+selenite-treated animals. The Ca(2+) level was significantly higher in Group 1 lenses compared to the amiloride-pretreated rats, but there was no significant difference between Groups 1 and 2 with regard to Na(+) and K(+) levels.
Amiloride was very effective in preventing cataract formation in the selenite-induced cataract model. This protective effect of amiloride was accompanied by higher glutathione levels and lower malondialdehyde levels in the rat pups' lenses compared to levels in animals that received selenite alone. These results suggest an anti-oxidant role for this agent, in addition to its effects on lens ion homeostasis.
确定氨氯吡咪对亚硒酸盐诱导的白内障的影响,确定该药物作为抗氧化剂的作用,并研究其对大鼠晶状体离子水平的相关影响。
将Wistar白化大鼠幼崽分为三组,一组为对照组,两组为实验组。第一实验组(第1组;n = 22)在出生后第10天皮下注射亚硒酸钠(30 nmol/g体重)。第二实验组(第2组;n = 21)在注射亚硒酸钠前15分钟皮下注射氨氯吡咪(1 nmol/g体重)。对照组(n = 22)不进行注射。在注射日期后的三周内观察每组幼崽。在此期间结束时,通过与裂隙灯照片比较确定白内障发展阶段,然后处死幼崽,并采用后路囊内摘除其晶状体。对每组进行阳离子分析并测量谷胱甘肽和丙二醛水平。
第1组的白内障阶段明显高于第2组。第1组和第2组的平均白内障阶段分别为3.8±0.12和1.6±0.25。对照组动物均未出现白内障。氨氯吡咪预处理组的谷胱甘肽水平明显高于第1组。第1组晶状体中的丙二醛水平约为第2组氨氯吡咪+亚硒酸盐处理动物晶状体的两倍。与氨氯吡咪预处理的大鼠相比,第1组晶状体中的Ca(2+)水平明显更高,但第1组和第2组在Na(+)和K(+)水平方面无显著差异。
在亚硒酸盐诱导的白内障模型中,氨氯吡咪对预防白内障形成非常有效。与单独接受亚硒酸盐的动物相比,氨氯吡咪的这种保护作用伴随着大鼠幼崽晶状体中更高的谷胱甘肽水平和更低的丙二醛水平。这些结果表明该药物除了对晶状体离子稳态有影响外,还具有抗氧化作用。