The Royal College of Surgeons (RCS) rat is an animal model for human autosomal recessive retinitis pigmentosa. As the retinas of these animals degenerate from two to six weeks after birth, posterior subcapsular cataracts (PSCs) develop, presumably in response to toxic lipid peroxides formed by degenerating rod outer segments. Morphologically, these PSCs are thought to be characterized by a proliferation of dysplastic bladder-like fibers, or Wedl cells, in the meridional region of the lens, that subsequently migrate to, and aggregate at, the posterior pole as the PSC. This report presents the results of correlative scanning (SEM) and transmission (TEM) electron microscopic as well as light microscopic (LM) analysis of the ultrastructure of RCS PSCs, SEM analysis of two, four and six week old lenses (n = 6-10 specimens per age group) demonstrated that the PSCs of RCS rats resulted from a growth malformation of the posterior fiber ends from four to six weeks. The PSC is composed of markedly enlarged and irregular posterior fiber ends aberrantly curved away from the polar axis toward the vitreous rather than overlapping and abutting to form suture branches within and between concentric growth shells. LM analysis revealed evidence of progressively more numerous, enlarged, and irregular, ovate cellular profiles at the posterior pole from four to six weeks. However, there was no evidence of Wedl cells either within the meridional row region or along a migratory path from the equator to the posterior pole at any age. TEM analysis confirmed that the size and abnormal shapes of cellular profiles were consistent with SEM analysis and that nuclei were never observed within the plaque. In addition, there was considerable variation in cytoplasmic densities between cells, Also, dense deposits were frequently noted between cells and beneath the capsule. The orientation of posterior fiber end profiles to the posterior capsule was 45, 70 and 90 degrees at respectively two, four and six weeks of age. These results show that RCS PSCs are a consequence of abnormal posterior fiber end growth culminating in a posterior opacity. (C) 1998 Academic Press.
