PubMed1989
The restitution of normal fibergenesis that occurs in stationary radiation cataracts provides a unique opportunity to study the cytopathomechanism of radiocataractogenesis. Previous attempts at investigating this phenomenon have been limited by the lack of an appropriate animal model. This report describes the induction of stationary radiation cataracts in postmetamorphic bullfrogs following ocular irradiation with a 10 Gy (1 Gy = 100 rads) dose of X-rays. The eyes of non-irradiated animals and animals irradiated with 25 Gy (an established dose known to induce progressive cataracts in frogs) served as controls. Animals were followed biomicroscopically and histopathologically over 79 weeks. As previously described, the cataracts developed in a dose-dependent manner. The 25 Gy irradiated lenses rapidly progressed to complete opacification (4+) by 26 weeks, while lenses exposed to 10 Gy advanced to the 2.5+ stage by 35 weeks and progressed no further. In the lower dose lenses, transparent cortex began to appear anteriorly and posteriorly between the capsule and opaque fibers at 45 weeks. As the clear fibers accumulated, the disrupted region came to occupy increasingly deeper cortex. Histologically, opacities in both groups were preceded by disorganization of the bow cytoarchitecture, meridional row disorganization, and the appearance in the lens epithelium of nuclear polymorphism, fragmented nuclei, micronuclei, clusters of nuclei, and abnormal mitotic figures. In the lenses exposed to the 25 Gy dose, this damage continued to worsen, so that the 4+ stage was characterized by extensive epithelial cell death, absence of the lens bow, degenerated fiber masses, and liquefied substrata. In contrast, prior to the appearance of transparent cortex in the 10 Gy group, the lens epithelial aberrations, are of the bow, and meridional row disorganization were all observed to improve. Further, by 69 weeks, the lens epithelium appeared as a largely homogeneous population, and the meridional rows and the are of the bow had become reestablished. The details of these observations and their possible relationship to the cytopathomechanism of radiation cataract formation are discussed.