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.