Evolution of damage in the lens after in vivo close to threshold exposure to UV-B radiation: Cytomorphological study of apoptosis

The purpose of the present study was to investigate cataractogenesis and recovery of lens damage after in vivo close to threshold ultraviolet (UV)-B radiation around 300 nm. Eighty six-week-old albino Sprague–Dawley rats were familiarized to a rat restrainer five days prior to exposure. Groups of non-anesthetized rats were exposed unilaterally to 8 kJ/m2 UVR-300 nm. The animals were sacrificed at 1, 7, 48 and 336 h following exposure. The lenses were extracted for imaging of dark-field lens macro anatomy and measurement of intensity of forward lens light scattering to quantify lens opacities. Three exposed lenses and one non-exposed lens from each time interval were examined with light and transmission electron microscopy (TEM). Macro anatomy and lens light scattering revealed that all contralateral non-exposed lenses were clear. The degree of lens opacity (difference in lens light scattering between exposed and non-exposed lenses) increased during the 336 h, reaching a plateau towards the end of the observation period. Light microscopy and TEM demonstrated that apoptotic features appeared in the epithelium already 1 h after UVR exposure, and small vacuoles were seen in the outer cortex. Epithelial damage occurs during the first 48 h after exposure and is followed by regenerative repair at 336 h post-exposure. Apoptotic epithelial cells were phagocytized by adjacent epithelial cells. Cortical fiber cells exhibited increasing damage throughout the observation period without any clear repair after 336 h. In conclusion, acute UVR-induced cataract is partly a reversible. Lens epithelium is a primary target for UVR exposure. Damage to cortical fiber cells remained irreversible.