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Evolution of damage in the lens after in vivo close to threshold exposure to UV-B radiation: cytomorphological study of apoptosis
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience. (Per Söderberg)
St. Erik’s Eye Hospital, Karolinska Institutet, Stockholm, Sweden . (Stefan Löfgren)
University of Houston College of Optometry, Houston, Texas, USA. (Jan Bergmanson)
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience. (Per Söderberg)
2010 (English)In: Experimental Eye Research, ISSN 0014-4835, E-ISSN 1096-0007, Vol. 91, no 3, 369-377 p.Article in journal (Refereed) Published
Abstract [en]

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 300nm. 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 8kJ/m(2) UVR-300nm. The animals were sacrificed at 1, 7, 48 and 336h 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 336h, reaching a plateau towards the end of the observation period. Light microscopy and TEM demonstrated that apoptotic features appeared in the epithelium already 1h after UVR exposure, and small vacuoles were seen in the outer cortex. Epithelial damage occurs during the first 48h after exposure and is followed by regenerative repair at 336h 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 336h. 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.

Place, publisher, year, edition, pages
2010. Vol. 91, no 3, 369-377 p.
Keyword [en]
lens, ultraviolet radiation, cataract, apoptosis, repair, light scattering, microscopy
National Category
Medical and Health Sciences
Research subject
URN: urn:nbn:se:uu:diva-129440DOI: 10.1016/j.exer.2010.06.009ISI: 000281500700007PubMedID: 20599969OAI: oai:DiVA.org:uu-129440DiVA: diva2:343780
Ophthalmic biophysics
Available from: 2010-08-17 Created: 2010-08-16 Last updated: 2010-12-03Bibliographically approved

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