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K. Galichanin, J. Wang, L. Meyer, S. Löfgren, V. Mody, Jr., P. G. Söderberg; Evolution of Cytomorphological Alterations and Repair of the Lens After in vivo Exposure to UV-B Radiation. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2274. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate cataractogenesis and recovery of lens damage after in vivo close to threshold UV-B radiation around 300 nm.
Eighty six-week-old albino Sprague-Dawley rats were familiarized to a rat restrainer seven days prior to exposure. Groups of rats were exposed unilaterally to 8 kJ/m2 UVR-300 nm, without anesthesia. 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 light scattering to quantify lens opacities. Three exposed lenses and one nonexposed lens from each time interval were examined with light microscopy.
Semithin sections of control lenses had a normal single layer of epithelial cells with regular architecture of the nuclear bow, and the lens fibers were packed and oriented in order. One hour after UVR exposure, irregular epithelial cells appeared occasionally in the central zone and no disturbances were found in other areas of the epithelium, while the outer posterior cortex showed small vacuoles. At 7 hours postexposure, abnormal cells were spread all over the epithelium and the posterior superficial lens fiber cells were swollen. At 48 hours after exposure, most epithelial cells contained nuclear and cytoplasmic condensations, exhibiting apoptotic-like appearance, and were aggregated in multiple layers. The nuclear bow was deteriorated and cortical fiber cells throughout appeared swollen, partly fused and contained vacuoles. After 336 hours, the central epithelium was normal while the density of subcapsular vacuoles present at the equator was higher than in 48 hour group. The cortex remained damaged.
Acute UVR-induced cataractogenesis is partly a reversible process. Maximum damage appears at 48 hours after exposure. Central epithelial cells are more tolerant to UVR than equatorial cells.
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