Bahmani Fereshteh, Bathaie S Zahra, Aldavood S Javid, Ghahghaei Arezou
Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Mol Vis. 2012;18:439-48. Epub 2012 Feb 11.
The purpose of this paper was to investigate the effect of the oral administration of L-glycine (Gly) on the development of diabetic cataract induced by streptozotocin (STZ) in rats.
Two groups of male Wistar rats were intraperitoneally injected with a single dose of STZ (65 mg/kg bodyweight). Then, one group of diabetic rats and a control group were administered with 1% of Gly in drinking water for three months, ad libitum. Cataract development was monitored biweekly through ophthalmoscope inspection and was classified into four stages. At the end of 12 weeks, the animals were sacrificed and some biochemical parameters were determined in their lenses. The parameters include advanced glycation end products (AGEs), glycated proteins, total and soluble protein, glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), aldose reductase (AR), and sorbitol dehydrogenase (SDH). Some parameters were also determined in the serum and blood of the rats.
Diabetic cataract gradually progressed in the STZ-administered group with no other treatment. Consequently, up to the end of the experiment, 2/3 of the animals in this group reached to the last stage of the cataract (mature cataract). The progress of this process was much slower in the diabetic group that was treated with Gly. At the end of the study, the visual cataract score was significantly lower in the diabetic group treated with Gly compared to those administered with STZ. Some lens parameters, including glycated proteins, AGEs, SOD, and AR activities, were increased while some others, including soluble and total protein, GSH level, and CAT activity, were decreased due to diabetes induction. After Gly treatment, all the above-named parameters had reverse changes except for the CAT activity. The SDH activity in the lenses had no changes due to diabetes or treatment. In addition, this treatment significantly decreased the amount of serum glucose (Glc), serum AGEs, and glycated hemoglobin (HbA1c) in the diabetic rats. Gly also increased the ferric reducing antioxidant power (FRAP) in the serum of diabetic rats. However, the decreased bodyweight of animals due to diabetes induction was not compensated by Gly administration. It is important to note that Gly had no effect on normal rat parameters.
The results indicated that the oral administration of Gly significantly delayed the onset and the progression of diabetic cataract in rats. These effects were due to its antiglycating action and to a lesser extent, due to the inhibition of oxidative stress and polyol pathway.
本文旨在研究口服L-甘氨酸（Gly）对链脲佐菌素（STZ）诱导的大鼠糖尿病性白内障发展的影响。
两组雄性Wistar大鼠腹腔注射单剂量STZ（65 mg/kg体重）。然后，一组糖尿病大鼠和一个对照组自由饮用含1% Gly的水，持续三个月。每两周通过检眼镜检查监测白内障的发展情况，并分为四个阶段。在12周结束时，处死动物并测定其晶状体中的一些生化参数。这些参数包括晚期糖基化终产物（AGEs）、糖化蛋白、总蛋白和可溶性蛋白、谷胱甘肽（GSH）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、醛糖还原酶（AR）和山梨醇脱氢酶（SDH）。还测定了大鼠血清和血液中的一些参数。
在未进行其他处理的STZ给药组中，糖尿病性白内障逐渐发展。因此，到实验结束时，该组中2/3的动物达到了白内障的最后阶段（成熟白内障）。在接受Gly治疗的糖尿病组中，这一过程的进展要慢得多。在研究结束时，与接受STZ治疗的糖尿病组相比，接受Gly治疗的糖尿病组的视力白内障评分显著更低。由于糖尿病的诱导，一些晶状体参数，包括糖化蛋白、AGEs、SOD和AR活性增加，而其他一些参数，包括可溶性和总蛋白、GSH水平和CAT活性则降低。Gly治疗后，除CAT活性外，上述所有参数均发生相反变化。晶状体中的SDH活性不受糖尿病或治疗的影响。此外，这种治疗显著降低了糖尿病大鼠的血清葡萄糖（Glc）、血清AGEs和糖化血红蛋白（HbA1c）的含量。Gly还增加了糖尿病大鼠血清中的铁还原抗氧化能力（FRAP）。然而，Gly给药并未补偿因糖尿病诱导导致的动物体重下降。需要注意的是，Gly对正常大鼠参数没有影响。
结果表明，口服Gly可显著延迟大鼠糖尿病性白内障的发病和进展。这些作用归因于其抗糖化作用，在较小程度上归因于对氧化应激和多元醇途径的抑制。
