Creighton M O, Trevithick J R, Mousa G Y, Percy D H, McKinna A J, Dyson C, Maisel H, Bradley R
Can J Ophthalmol. 1978 Jul;13(3):166-81.
We examined 9 cataracts from maturity onset diabetics and 4 senile posterior subcapsular cataracts by scanning electron microscopy, transmission electron microscopy, immunofluorescence for crystallin proteins and actin, histochemical methods and x-ray diffraction. The cataractous regions contained spherical globules up to 20 mu in diameter, often in a fibrous matrix. Some were extracellular Morgagnian globules, apparently formed by blebbing from the cell surface; others appeared to have been formed intracellularly. The area of globular degeneration was usually 300 mu deep, but had deeper fusiform extensions. Morphological changes in the cell cytoplasm varied according to their depth in the cataract. Electron microscopy showed intracellular and extracellular globules, many of them were bounded by lipid bilayer membranes. Immunofluorescent staining showed that all the globules contained gamma-crystallin; some contained alpha- and beta-crystallins and actin. All the globules contained higher concentrations of cysteine or cystine than the surrounding lens tissue but they did not react to stains for carbohydrate or calcium. X-ray diffraction studies showed that crystalline calcium salts were absent. Globules and cavities averaged 45% of the total area in cross section. Assuming an area of cataract to be 300 micron thick and that globules 1 mu in diameter scattered, while 2--20 mu in diameter reflected light, we calculated that light passing through such a thickness would be reduced by 65%. Thus the globules could account for most of the opacity of the cataractous area. Presumably the fibrous degeneration of the cells causes enough light scattering to account for the remainder of the reduction. Cataract patients complain of decreased visual acuity, a golden halo around objects, and difficulties when driving while facing oncoming traffic at night. These probably result from light scattering. In our previous experiments, globular bodies containing gamma-crystallin were found in cells grown in tissue culture, and blebs with increased acitn content similar to Morgagnian globules were formed in tissue culture by treating differentiated rat lens cells of stage 2 by cytochalasin D (which impaired microfilament function). These results suggest the possibility of simulating in tissue culture the morphological alterations seen in the cataractous cell.
我们通过扫描电子显微镜、透射电子显微镜、晶状体蛋白和肌动蛋白的免疫荧光、组织化学方法及X射线衍射，对9例成年起病型糖尿病患者的白内障及4例老年性后囊下白内障进行了检查。白内障区域含有直径达20微米的球形小体，常存在于纤维基质中。一些是细胞外的莫尔加尼小体，显然是由细胞表面的泡状突起形成；另一些似乎是在细胞内形成的。球状变性区域通常深300微米，但有更深的梭形延伸。细胞质的形态变化根据其在白内障中的深度而有所不同。电子显微镜显示细胞内和细胞外小体，其中许多被脂质双分子层膜包围。免疫荧光染色显示所有小体都含有γ-晶状体蛋白；一些还含有α-和β-晶状体蛋白以及肌动蛋白。所有小体中半胱氨酸或胱氨酸的浓度都高于周围晶状体组织，但它们对碳水化合物或钙的染色无反应。X射线衍射研究表明不存在结晶性钙盐。小体和腔隙在横切面上平均占总面积的45%。假设白内障区域厚300微米，直径1微米的小体散射光线，而直径2 - 20微米的小体反射光线，我们计算得出穿过这样厚度的光线会减少65%。因此，这些小体可能是白内障区域大部分不透明的原因。据推测，细胞的纤维变性导致足够的光散射，从而解释了其余的光线减少。白内障患者抱怨视力下降、物体周围有金色光环以及夜间面对迎面而来的车辆驾驶时困难。这些可能是由光散射引起的。在我们之前的实验中，在组织培养的细胞中发现了含有γ-晶状体蛋白的球状体，并且通过用细胞松弛素D（它损害微丝功能）处理2期分化的大鼠晶状体细胞，在组织培养中形成了与莫尔加尼小体类似的肌动蛋白含量增加的泡状突起。这些结果表明在组织培养中模拟白内障细胞中所见形态改变的可能性。
