March 1999
Volume 40, Issue 3
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Articles  |   March 1999
Anterior polar cataracts in CS rats: a predictor of mature cataract formation.
Author Affiliations
  • K J Al-Ghoul
    Department of Pathology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois 60612, USA.
  • J R Kuszak
    Department of Pathology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois 60612, USA.
Investigative Ophthalmology & Visual Science March 1999, Vol.40, 668-679. doi:
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      K J Al-Ghoul, J R Kuszak; Anterior polar cataracts in CS rats: a predictor of mature cataract formation.. Invest. Ophthalmol. Vis. Sci. 1999;40(3):668-679.

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Abstract

PURPOSE: The objective of this study was to characterize the morphology of the anterior opacities formed during recovery from posterior subcapsular cataract (PSC) in Royal College of Surgeons (RCS) rats. METHODS: Lenses from RCS rats at 8 and 12 weeks postnatal (n = 14 and 12, respectively) were examined under a dissecting microscope for the presence of anterior opacities. Lenses with anterior opacities were fixed, embedded in epoxy resin, and sectioned along the optic axis for light microscopy (LM) and transmission electron microscopy (TEM). RESULTS: At eight weeks postnatal, 21.5% of animals (3/14) had anterior cataracts. Light microscopy of 1- to 2-microm-thick sections revealed an anomalous layer of material located at the epithelium-fiber interface, which was identified as a zone of liquefaction by TEM. Epithelial cells had minor structural defects but were not necrotic. Anterior portions of elongating and cortical fibers under the zone of liquefaction were undisrupted, whereas their posterior portions had numerous vacuoles. The anterior opacities were classified as anterior polar cataracts (APCs) based on the location and type of morphologic damage in the affected lenses. At twelve weeks postnatal, 25% of animals (3/12) had APCs that involved prominent vesiculation of the anterior cortex. Ultrastructural examination showed that large vesicles were located between and inside anterior fibers and that most extracellular spaces were abnormally widened. Posteriorly, internalization of the PSC by new fiber growth was disordered and displayed vesiculation and density variations. In the bow region, LM revealed minor structural irregularities that were identified as groups of apparently degenerating fibers by TEM. CONCLUSIONS: APCs in RCS rats are caused by degeneration of elongating fibers in the bow region and subsequent damage in the superficial anterior cortex. The percentage of animals with APCs (25%) was consistent with the percentage of animals in which mature cataracts eventually develop. The morphologic changes, time of onset, and percentage of animals affected suggest that APC is the initial manifestation of mature cataract formation in RCS rats.

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