Hightower K R, McCready J P, Borchman D
Eye Research Institute, Oakland University, Rochester, MI 48309.
Photochem Photobiol. 1994 Apr;59(4):485-90. doi: 10.1111/j.1751-1097.1994.tb05069.x.
The purpose of this study was to investigate three possible causes of membrane damage following UV irradiation: photooxidation of membrane thiol (SH) groups, peroxidation of membrane lipids and inhibited synthesis of membrane proteins. Thiol loss was not observed. Thin-layer chromatography showed a four-fold increase in several primary lipid peroxidation products such as hydroperoxyl lipids in the epithelial membrane preparations isolated from irradiated lenses. The formation of new hydroxyl lipid bands not seen in control preparations was also observed in isolated membranes from irradiated lenses. Irradiation in the presence or absence of oxygen produced lipid peroxidation products. Aerobic irradiation produced small, but statistically significant increases in lipid hydroxyls and hydroperoxyls relative to controls. Repair of initial damage might be compromised by the observed 60% reduction in rate of protein synthesis measured in lens membranes following irradiation. Synthesis was affected by means other than depleted potassium or elevated calcium levels.
膜硫醇（SH）基团的光氧化、膜脂质的过氧化和膜蛋白合成的抑制。未观察到硫醇损失。薄层色谱显示，从受辐照晶状体分离的上皮膜制剂中，几种主要脂质过氧化产物如氢过氧基脂质增加了四倍。在受辐照晶状体的分离膜中也观察到了对照制剂中未见的新的羟基脂质带的形成。在有氧或无氧条件下照射都会产生脂质过氧化产物。与对照相比，有氧照射使脂质羟基和氢过氧基有小幅但在统计学上显著的增加。照射后晶状体膜中蛋白质合成速率降低了60%，这可能会影响初始损伤的修复。合成受到除钾离子耗尽或钙离子水平升高以外的其他因素影响。
