IOVS Molecular Pharmacology
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(Investigative Ophthalmology and Visual Science. 2000;41:204-212.)
© 2000 by The Association for Research in Vision and Ophthalmology, Inc.

Repair in the Rat Lens after Threshold Ultraviolet Radiation Injury

Ralph Michael1,2, Gijs F. J. M. Vrensen2,3, Jan van Marle4, Stefan Löfgren1 and Per G. Söderberg1

1 From the Karolinska Institutet, St. Erik’s Eye Hospital, Stockholm, Sweden; 2 The Netherlands Ophthalmic Research Institute, Amsterdam; 3 Department of Ophthalmology, State University of Leiden; and 4 Department of Electron Microscopy, Amsterdam Medical Center, University of Amsterdam, The Netherlands.

PURPOSE. To investigate the development and recovery of lens damage after in vivo close-to-threshold exposure to ultraviolet B radiation.

METHODS. One eye of young, female Sprague–Dawley rats was exposed to 5 kJ/m2 narrowband ultraviolet radiation (UVR) ({lambda}max = 302 nm) for 15 minutes. Groups of rats were killed 1, 7, and 56 days after exposure. The structure of the exposed and nonexposed lenses was examined with light microscopy, scanning electron microscopy, transmission electron microscopy, freeze–fracture, fluorescent membrane staining, and Fourier transform analysis.

RESULTS. One day after UVR exposure the lens surface had flakelike opacities. Seven days after exposure, the lens surface appeared opaque and corrugated, and the equatorial cortex had small opacities. At 56 days postexposure, the surface and equator appeared clear, but the cortex had a subtle shell-shaped opacity. At 1 day postexposure, apoptotic cell death occurred in the lens epithelium, but the cortical fibers were normal. At 7 days postexposure, the epithelium and the fibers between the 10th and 40th growth shell below the capsule contained extracellular spaces of different sizes. After 56 days, the epithelial layer appeared normal, and the extracellular spaces had disappeared; but abnormal fibers were found between the 60th and 100th growth shell below the capsule. Fibers above and below the damaged growth shells appeared fully normal.

CONCLUSIONS. A close-to-threshold dose of UVR causes cataract, which is largely reversible. The UVR exposure leads to apoptosis in the lens epithelium, and after a latency period of several days, lens fibers are abnormal. Extracellular spaces develop in the epithelium and fibers. Within several weeks after exposure, the epithelium fully recovers and new fibers develop normally. The originally affected fibers are repaired. However, this repair is incomplete, leaving a small zone of enhanced light scattering in the equatorial cortex.




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