Department of Ophthalmology, Tangdu Hospital, Xi'an, China.
Curr Eye Res. 2013 Jun;38(6):639-48. doi: 10.3109/02713683.2012.760741. Epub 2013 Mar 27.
The aim of the study was to investigate the protective effects of intact vitreous gel on the lens after pharmacologic vitreolysis and hyperoxia exposure in rats in vivo.
Eyes of Sprague-Dawley rats were induced to posterior vitreous detachment (PVD) by pharmacologic vitreolysis, and the rats with and without PVD were treated with hyperoxia 3 h per day for 5 months. Lens transparency was monitored by a slit-lamp biomicroscope. A series of biochemical measurements were made in extracts of the lens cortex and nucleus. Ascorbate levels were measured in the aqueous and vitreous humors.
No significant differences in lens transparency or morphology were observed in all groups, and no significant biochemical changes were observed in the cortex or nucleus of lenses of the PVD group. In the lens nucleus, the values of water-soluble protein concentration in PVD + hyperoxia group were lower than that of the PVD group. The levels of water-soluble proteins, glutathione (GSH) and ascorbate decreased in the hyperoxia group with an intact vitreous body. Vitreolysis enhanced the effect of hyperoxia, decreasing soluble protein, GSH and ascorbate below the levels seen in eyes with vitreolysis alone. The levels of antioxidants and soluble proteins were lower in the lens nucleus, and the effects of vitreolysis plus hyperoxia were more significant in the nucleus. Hyperoxia and hyperoxia plus vitreolysis reduced catalase activity and increased oxidized GSH to a greater extent in the lens cortex, although these treatments increased protein-GSH mixed disulfides in both regions. Long-term hyperoxia also lowered ascorbate levels in the vitreous and aqueous humors, an effect that was enhanced by vitreolysis.
Exposure to excess molecular oxygen produces significant oxidative damage to the lens, especially the lens nucleus. These effects were enhanced by pharmacologic vitreolysis, indicating that intact vitreous gel protects the lens from oxidative damage.
本研究旨在探讨玻璃体凝胶完整状态对体内药物性玻璃体液化和高氧暴露后晶状体的保护作用。
采用药物性玻璃体液化诱导 Sprague-Dawley 大鼠产生后玻璃体脱离（PVD），并对 PVD 大鼠和无 PVD 大鼠每天进行 3 小时的高氧处理，持续 5 个月。通过裂隙灯生物显微镜监测晶状体透明度。对晶状体皮质和核提取物进行了一系列生化测量。测量了房水和玻璃体中的抗坏血酸水平。
所有组别的晶状体透明度或形态均无显著差异，PVD 组晶状体皮质和核无显著生化变化。在晶状体核中，PVD+高氧组水溶性蛋白浓度值低于 PVD 组。高氧组的水溶性蛋白、谷胱甘肽（GSH）和抗坏血酸水平下降，玻璃体完整的情况下则更低。玻璃体液化增强了高氧的作用，使可溶性蛋白、GSH 和抗坏血酸水平低于单纯玻璃体液化的水平。晶状体核中的抗氧化剂和可溶性蛋白水平较低，玻璃体液化联合高氧的作用更为显著。高氧和高氧联合玻璃体液化使晶状体皮质中的过氧化氢酶活性降低，氧化型 GSH 增加，尽管这两种处理都增加了两个区域的蛋白-GSH 混合二硫化物。长期高氧也降低了玻璃体和房水中的抗坏血酸水平，这种作用在玻璃体液化的情况下更为明显。
暴露于过量的分子氧会对晶状体造成显著的氧化损伤，特别是晶状体核。这些作用通过药物性玻璃体液化而增强，表明完整的玻璃体凝胶可保护晶状体免受氧化损伤。
