Repair in the rat lens after threshold ultraviolet radiation injury

Citation
R. Michael et al., Repair in the rat lens after threshold ultraviolet radiation injury, INV OPHTH V, 41(1), 2000, pp. 204-212
Citations number
39
Categorie Soggetti
da verificare
Journal title
INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
ISSN journal
01460404 → ACNP
Volume
41
Issue
1
Year of publication
2000
Pages
204 - 212
Database
ISI
SICI code
0146-0404(200001)41:1<204:RITRLA>2.0.ZU;2-O
Abstract
PURPOSE. To investigate the development and recovery of lens damage after i n vivo close-to-threshold exposure to ultraviolet B radiation. METHODS. One eye of young, female Sprague-Dawley rats was exposed to 5 kJ/m (2) narrowband ultraviolet radiation (UVR) (lambda(max) = 302 nm) for 15 mi nutes. Groups of rats were killed 1, 7, and 56 days after exposure. The str ucture of the exposed and nonexposed lenses was examined with light microsc opy, 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 opacitie s. Seven days after exposure, the lens surface appeared opaque and corrugat ed, 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. Ar 1 day postexposure, apoptotic cell death occurred in the lens epithelium, but the cortical fibers were normal. At 7 days postexposu re, the epithelium and the fibers between the 10th and 40th growth shell be low the capsule contained extracellular spaces of different sizes. After 56 days, the epithelial layer appeared normal, and the extracellular spaces h ad disappeared; but abnormal fibers were found between the 60th and 100th g rowth shell below the capsule. Fibers above and below the damaged growth sh ells appeared fully normal. CONCLUSIONS. A close-to-threshold dose of UVR causes cataract, which is lar gely reversible. The UVR exposure lends to apoptosis in the lens epithelium , and after a latency period of several days, lens fibers are abnormal. Ext racellular spaces develop in the epithelium and fibers. Within several week s after exposure, the epithelium fully recovers and new fibers develop norm ally. The originally affected fibers are repaired. However, this repair is incomplete. leaving a small zone of enhanced light scattering in the equato rial cortex.